To see the other types of publications on this topic, follow the link: Intestine, Small Immunology.
Journal articles on the topic 'Intestine, Small Immunology'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Intestine, Small Immunology.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Bland, P. W., and M. Bailey. "Immunology of the small intestine." Transplantation Proceedings 30, no. 6 (September 1998): 2560–61. http://dx.doi.org/10.1016/s0041-1345(98)00725-8.
Full text
2
Kunisawa, Jun, Yosuke Kurashima, Morio Higuchi, Masashi Gohda, Izumi Ishikawa, Ikuko Ogahara, Namju Kim, Miki Shimizu, and Hiroshi Kiyono. "Small and large intestinal intraepithelial T lymphocytes show distinct dependency on sphingosine 1-phosphate (42.11)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S35. http://dx.doi.org/10.4049/jimmunol.178.supp.42.11.
Full textAbstract:
Abstract It is known that the composition of intraepithelial T lymphocyte (IEL) differs between small and large intestines, but the mechanism underlying that difference remains obscure. Here, we show that sphingosine 1-phosphate (S1P) plays a key role in regulating intestinal IEL trafficking into the small and large intestines. High levels of type 1 S1P receptor (S1P1) expression was noted on naïve IELs expressing CD4 or CD8αβ, which leads to their preferential migration into the large intestine. In contrast, recent thymic emigrants (RTEs), double-positive thymocytes, and double-negative thymic T cell-committed precursors use S1P-independent trafficking pathway into the intestine. The former two populations exclusively migrate into the small intestine, while the latter double-negative thymic T cell-committed precursors migrate into both the small and large intestines. Hence, down-regulation of S1P1 expression inhibited naïve IEL migration into the intestines but did not affect the migration of thymic IEL precursors. These data are the first to demonstrate that a lipid-mediated system determines whether IELs migrate to the small or large intestine.
3
Brandl, Katharina, George Plitas, Ronald P. DeMatteo, Laura V. Hooper, and Eric G. Pamer. "MyD88-mediated signals induce in vivo production of the bactericidal lectin RegIIIγ and protect against intestinal Listeria monocytogenes infection (44.4)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S48. http://dx.doi.org/10.4049/jimmunol.178.supp.44.4.
Full textAbstract:
Abstract Listeria monocytogenes (L. monocytogenes) is an intracellular bacterium that causes systemic infections after traversing the intestinal mucosa. To test the hypothesis that the Toll-like receptor pathway is involved in defense against intestinal L. monocytogenes infection, we analyzed the role of the common intracellular adaptor molecule myeloid differentiation primary-response protein 88 (MyD88) following oral infection with L. monocytogenes. We found that MyD88 deficient mice have increased susceptibility to intestinal L. monocytogenes infection with higher bacterial burden in spleen, liver, mesenteric lymph nodes, intestinal lumen, and small intestine (lamina propria and intestinal epithelium). Further in vitro and in vivo studies showed that MyD88 mediated protection primarily occurs in the distal small intestine. Recently, it was shown that the intestinal bactericidal lectin RegIIIγ has antibacterial activity against L. monocytogenes. RT-PCR and Western Blot analysis of distal small intestines showed that RegIIIγ is significantly diminished in MyD88 deficient mice. Since optimal expression of RegIIIγ requires MyD88-mediated signals, our findings suggest that increased susceptibility to intestinal L. monocytogenes infection in MyD88-deficient mice results from diminished levels of this bactericidal lectin in the distal small bowel.
4
Chowers, Y., W. Holtmeier, J. Harwood, E. Morzycka-Wroblewska, and M. F. Kagnoff. "The V delta 1 T cell receptor repertoire in human small intestine and colon." Journal of Experimental Medicine 180, no. 1 (July 1, 1994): 183–90. http://dx.doi.org/10.1084/jem.180.1.183.
Full textAbstract:
V delta 1 bearing T cells comprise the major population of gamma/delta T cells in the human intestinal tract. To gain insight into mechanisms involved in the generation of these cells and the diversity of their repertoire, we have characterized the junctional sequences of V delta 1 T cell receptor transcripts in the human small intestine and colon. Mucosal biopsies obtained from defined regions along the length of the small intestine or colon contained a high frequency of either one or a few identical in frame V delta 1 sequences. Less abundant sequences were also detected repeatedly throughout the length of small intestine or colon. Moreover, the intestinal V delta 1 repertoire in the small intestine and colon appeared compartmentalized and showed no overlap with the V delta 1 repertoire in peripheral blood. Dominant V delta 1 transcripts in each subject differed between the small intestine and colon, and the dominant transcripts within these sites differed among individuals. Analysis of small intestinal transcripts obtained at a 1-yr interval revealed that the V delta 1 repertoire was stable over time. The fact that the majority of V delta 1 transcripts, both dominant and rare, are distributed throughout a several meter length of the adult intestinal tract and are stable over time suggests they are not generated by an ongoing process of in situ VDJ gene rearrangement. Our results favor a model in which the repertoire of V delta 1 T cells in the intestinal tract is shaped by positive selection in response to a limited array of ligands before the migration of V delta 1 cells throughout the small intestine or colon.
5
Beagley, K. W., K. Fujihashi, A. S. Lagoo, S. Lagoo-Deenadaylan, C. A. Black, A. M. Murray, A. T. Sharmanov, M. Yamamoto, J. R. McGhee, and C. O. Elson. "Differences in intraepithelial lymphocyte T cell subsets isolated from murine small versus large intestine." Journal of Immunology 154, no. 11 (June 1, 1995): 5611–19. http://dx.doi.org/10.4049/jimmunol.154.11.5611.
Full textAbstract:
Abstract Intraepithelial lymphocytes (IELs) have been extensively studied in the murine small intestine. However, to date no studies have assessed IEL in the large intestine, despite the marked differences in function and lumenal environment. In the present study, we isolated IEL from both small and large intestine of three mouse strains (BALB/c, C3H/HeN, C57BL/6) and determined the frequency of CD2, CD4, and CD8 expression on CD3+ IEL, as well as the frequency of alpha beta and gamma delta TCR usage and V beta distribution. Higher numbers of IEL/unit length were always isolated from the small intestine (20-30 x 10(6)/5 mice) compared with large intestine (1.1-2.5 x 10(6)/5 mice). Interestingly, IEL from the large intestine of all strains were predominantly alpha beta TCR+ whereas gamma delta TCR+ IELs predominated in small intestine. Large intestinal IELs were mainly CD4+, in both BALB/c and C3H/HeN mouse strains. IELs from large intestine of C57BL/6 mice were mainly CD8+; however, the CD4+ subset was fourfold higher when compared with small intestine IEL. Potential functional differences between IEL subsets was assessed by determining the relative levels of mRNA for IL-1, 2, 4, 5, 10, IFN-gamma, TGF-beta, and TNF-gamma. Similar patterns of IL-1, IFN-gamma and TNF-alpha were seen while more IL-2, IL-4, IL-5, and IL-10 mRNA was noted in large intestinal IEL. Stimulation of C3H/HeJ IEL with anti-CD3 also resulted in higher levels of IL-3/GM-CSF, IL-4, and IL-6 by IEL from large intestine. These results show that marked differences occur among the T cell subsets present in IELs from mouse small and large intestine.
6
Allenspach, Karin. "Clinical Immunology and Immunopathology of the Canine and Feline Intestine." Veterinary Clinics of North America: Small Animal Practice 41, no. 2 (March 2011): 345–60. http://dx.doi.org/10.1016/j.cvsm.2011.01.004.
Full text
7
Limon, Natalie M. "The Effects of Childhood, Adolescent and Adult Obesity on Epithelial T Cell Homeostasis in the Intestine." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 211.10. http://dx.doi.org/10.4049/jimmunol.198.supp.211.10.
Full textAbstract:
Abstract According to the CDC, 30% of adults in the U.S population are obese, while 17% of children and adolescents are obese. Obesity has resulted in a wide array of complications including disruption of barrier permeability as well as problems with tissue repair. The epithelial layer of the intestines contains intraepithelial intestinal lymphocytes (IEL) that are important in maintaining epithelial homeostasis and repairing tissue. To outline the mechanism by which obesity disrupts intestinal epithelial function among different age groups, childhood, adolescent, and adult mice were placed in a high fat diet (HFD) for 7 weeks to observe IEL number and function. In all age groups, mice administered a HFD exhibit a significant decrease in IEL within the epithelial layer of the small intestine. Notably, in the childhood cohort, IEL seeding is disrupted resulting in limited IEL numbers during adolescence. Interestingly, T cells in the epidermis of the skin are not reduced in number after 7 weeks of HFD suggesting that the intestine is more sensitive to early obesity. This study shows the harmful impact of obesity on the immune system in the small intestine whether obesity occurs in youth or in adulthood.
8
Wang, Jian, Fengqi Li, Haiming Wei, Zhe-Xiong Lian, Rui Sun, and Zhigang Tian. "Respiratory influenza virus infection induces intestinal immune injury via microbiota-mediated Th17 cell–dependent inflammation." Journal of Experimental Medicine 211, no. 12 (November 3, 2014): 2397–410. http://dx.doi.org/10.1084/jem.20140625.
Full textAbstract:
Influenza in humans is often accompanied by gastroenteritis-like symptoms such as diarrhea, but the underlying mechanism is not yet understood. We explored the occurrence of gastroenteritis-like symptoms using a mouse model of respiratory influenza infection. We found that respiratory influenza infection caused intestinal injury when lung injury occurred, which was not due to direct intestinal viral infection. Influenza infection altered the intestinal microbiota composition, which was mediated by IFN-γ produced by lung-derived CCR9+CD4+ T cells recruited into the small intestine. Th17 cells markedly increased in the small intestine after PR8 infection, and neutralizing IL-17A reduced intestinal injury. Moreover, antibiotic depletion of intestinal microbiota reduced IL-17A production and attenuated influenza-caused intestinal injury. Further study showed that the alteration of intestinal microbiota significantly stimulated IL-15 production from intestinal epithelial cells, which subsequently promoted Th17 cell polarization in the small intestine in situ. Thus, our findings provide new insights into an undescribed mechanism by which respiratory influenza infection causes intestinal disease.
9
Hong, Chun Pyo, Bo Gie Yang, Jung-Hwan Kim, Min Seong Jang, Eun-Jung Lee, Eun Ji Jeun, Chan Kim, Ju-Young Seoh, and Myoung Ho Jang. "High fat diet-induced obesity affects CD4+ T cell differentiation in the small intestine (P3176)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 61.13. http://dx.doi.org/10.4049/jimmunol.190.supp.61.13.
Full textAbstract:
Abstract Obesity-induced metabolic diseases are caused by the excess infiltration of pro-inflammatory cells to metabolic tissues including adipose and liver. However, systematic understanding of correlation between obesity and alterations of gut immunity is unclear. We hypothesized that immune cells in small intestine may be affected substantially upon high-fat feeding since dietary lipids are absorbed at luminal surface of small intestine. Here we found that small intestinal CD4+ and CD8+ T cells but not B cells were decreased in obese state. In CD4+ T cell subsets, the proportion of TH1 cells was increased in obese state, whereas the proportion of TH17 cells was decreased. The regulation of Intestinal T cells is dependent on antigen presenting cells such as macrophages and dendritic cells. We found intestinal macrophage subsets but not dendritic cells were changed in obese state. We next investigated that which antigen presenting cells from small intestine control CD4+ T cell differentiation during obese state ex vivo. We found that two macrophage subsets control balance of TH1 and TH17 cells inversely. These results show that small intestinal macrophages can have a key role in modulating small intestinal CD4+ T cell differentiation during obesity.
10
Vidal, Jorge E., Bruce A. McClane, Juliann Saputo, Jaquelyn Parker, and Francisco A. Uzal. "Effects of Clostridium perfringens Beta-Toxin on the Rabbit Small Intestine and Colon." Infection and Immunity 76, no. 10 (July 14, 2008): 4396–404. http://dx.doi.org/10.1128/iai.00547-08.
Full textAbstract:
ABSTRACT Clostridium perfringens type B and type C isolates, which produce beta-toxin (CPB), cause fatal diseases originating in the intestines of humans or livestock. Our previous studies demonstrated that CPB is necessary for type C isolate CN3685 to cause bloody necrotic enteritis in a rabbit ileal loop model and also showed that purified CPB, in the presence of trypsin inhibitor (TI), can reproduce type C pathology in rabbit ileal loops. We report here a more complete characterization of the effects of purified CPB in the rabbit small and large intestines. One microgram of purified CPB, in the presence of TI, was found to be sufficient to cause significant accumulation of hemorrhagic luminal fluid in duodenal, jejunal, or ileal loops treated for 6 h with purified CPB, while no damage was observed in corresponding loops receiving CPB (no TI) or TI alone. In contrast to the CPB sensitivity of the small intestine, the colon was not affected by 6 h of treatment with even 90 μg of purified CPB whether or not TI was present. Time course studies showed that purified CPB begins to induce small intestinal damage within 1 h, at which time the duodenum is less damaged than the jejunum or ileum. These observations help to explain why type B and C infections primarily involve the small intestine, establish CPB as a very potent and fast-acting toxin in the small intestines, and confirm a key role for intestinal trypsin as an innate intestinal defense mechanism against CPB-producing C. perfringens isolates.
11
Miller, Mark, Jack Xu, Jeremiah McDole, Keely McDonald, Kathryn Knoop, and Rodney Newberry. "Toll-like receptor signaling regulates mucosal barrier function and antigen acquisition in the small intestine (P3266)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 136.15. http://dx.doi.org/10.4049/jimmunol.190.supp.136.15.
Full textAbstract:
Abstract The mucosal immune system must efficiently recognize foreign antigen during intestinal infection and yet avoid triggering inappropriate inflammatory responses to commensal microbes and food antigens. In vivo two-photon imaging revealed that low-molecular weight material can cross the epithelium of the small intestine during goblet cell secretion, a phenomenon termed goblet cell-associated antigen passages (GAPs). GAPs are abundant in the steady-state and selectively deliver foreign antigen to CD103+ lamina propria dendritic cells with tolerogenic potential. However, under pathological conditions, goblet cell secretion and epithelial permeability are dramatically altered. The cellular mechanisms that regulate barrier function in response to luminal microbial products are poorly understood, but have important ramifications for intestinal pathogenesis and oral vaccine efficacy. We found that Toll-like receptor (TLR) ligands introduced acutely into the intestines of germ free mice modulated GAP formation in vivo. Furthermore, mice deficient in TLRs that signal through TRIF, lacked GAPs and had reduced epithelial permeability. We propose that a subset of villus epithelial cells expressing TLR3/TLR4 and containing high levels of serotonin (5HT) can induce GAP formation in the small intestine by secreting 5HT in response to TLR ligands.
12
Sugawara, Reiko, Eun-Jung Lee, Min Seong Jang, Eun-Ji Jeun, Chun-Pyo Hong, Jung-Hwan Kim, Areum Park, et al. "Small intestinal eosinophils regulate Th17 cells by producing IL-1 receptor antagonist." Journal of Experimental Medicine 213, no. 4 (March 7, 2016): 555–67. http://dx.doi.org/10.1084/jem.20141388.
Full textAbstract:
Eosinophils play proinflammatory roles in helminth infections and allergic diseases. Under steady-state conditions, eosinophils are abundantly found in the small intestinal lamina propria, but their physiological function is largely unexplored. In this study, we found that small intestinal eosinophils down-regulate Th17 cells. Th17 cells in the small intestine were markedly increased in the ΔdblGATA-1 mice lacking eosinophils, and an inverse correlation was observed between the number of eosinophils and that of Th17 cells in the small intestine of wild-type mice. In addition, small intestinal eosinophils suppressed the in vitro differentiation of Th17 cells, as well as IL-17 production by small intestinal CD4+ T cells. Unlike other small intestinal immune cells or circulating eosinophils, we found that small intestinal eosinophils have a unique ability to constitutively secrete high levels of IL-1 receptor antagonist (IL-1Ra), a natural inhibitor of IL-1β. Moreover, small intestinal eosinophils isolated from IL-1Ra−deficient mice failed to suppress Th17 cells. Collectively, our results demonstrate that small intestinal eosinophils play a pivotal role in the maintenance of intestinal homeostasis by regulating Th17 cells via production of IL-1Ra.
13
Donaldson, David S., Kathryn J. Else, and Neil A. Mabbott. "The Gut-Associated Lymphoid Tissues in the Small Intestine, Not the Large Intestine, Play a Major Role in Oral Prion Disease Pathogenesis." Journal of Virology 89, no. 18 (July 8, 2015): 9532–47. http://dx.doi.org/10.1128/jvi.01544-15.
Full textAbstract:
ABSTRACTPrion diseases are infectious neurodegenerative disorders characterized by accumulations of abnormally folded cellular prion protein in affected tissues. Many natural prion diseases are acquired orally, and following exposure, the early replication of some prion isolates upon follicular dendritic cells (FDC) within gut-associated lymphoid tissues (GALT) is important for the efficient spread of disease to the brain (neuroinvasion). Prion detection within large intestinal GALT biopsy specimens has been used to estimate human and animal disease prevalence. However, the relative contributions of the small and large intestinal GALT to oral prion pathogenesis were unknown. To address this issue, we created mice that specifically lacked FDC-containing GALT only in the small intestine. Our data show that oral prion disease susceptibility was dramatically reduced in mice lacking small intestinal GALT. Although these mice had FDC-containing GALT throughout their large intestines, these tissues were not early sites of prion accumulation or neuroinvasion. We also determined whether pathology specifically within the large intestine might influence prion pathogenesis. Congruent infection with the nematode parasiteTrichuris murisin the large intestine around the time of oral prion exposure did not affect disease pathogenesis. Together, these data demonstrate that the small intestinal GALT are the major early sites of prion accumulation and neuroinvasion after oral exposure. This has important implications for our understanding of the factors that influence the risk of infection and the preclinical diagnosis of disease.IMPORTANCEMany natural prion diseases are acquired orally. After exposure, the accumulation of some prion diseases in the gut-associated lymphoid tissues (GALT) is important for efficient spread of disease to the brain. However, the relative contributions of GALT in the small and large intestines to oral prion pathogenesis were unknown. We show that the small intestinal GALT are the essential early sites of prion accumulation. Furthermore, congruent infection with a large intestinal helminth (worm) around the time of oral prion exposure did not affect disease pathogenesis. This is important for our understanding of the factors that influence the risk of prion infection and the preclinical diagnosis of disease. The detection of prions within large intestinal GALT biopsy specimens has been used to estimate human and animal disease prevalence. However, our data suggest that using these biopsy specimens may miss individuals in the early stages of oral prion infection and significantly underestimate the disease prevalence.
14
Stefka, Andrew T., Maria EC Bruno, and Charlotte S. Kaetzel. "MyD88-dependent regulation of the polymeric immunoglobulin receptor by colonic microbes (40.5)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S28. http://dx.doi.org/10.4049/jimmunol.178.supp.40.5.
Full textAbstract:
Abstract Secretory IgA serves as the first line of antigen-specific immunity in the intestine, protecting against pathogens while preventing inflammation in response to commensal microbes. Intestinal epithelial cells (IEC) regulate IgA secretion by controlling expression of the polymeric immunoglobulin receptor (pIgR). Many pro- and anti-inflammatory factors, including pIgR, are transcriptional targets of Toll-like receptor (TLR) signaling in response to molecular patterns from resident microbes. MyD88 is an important TLR signaling adaptor that has been implicated in regulation of intestinal inflammation. To assess the role of MyD88 in IEC gene expression, we compared mRNA levels of pIgR, TNF, and two regulatory factors, A20 and MKP-1, in the small intestines and colons of wild-type and MyD88−/− mice. Gene expression was significantly higher in the colon than in the small intestine of all mice, correlating with the higher microbial load. In the colon, expression of all genes was significantly higher in wild-type than in MyD88−/−mice. We conclude that commensal microorganisms set the tone of intestinal gene expression through MyD88-dependent TLR signaling. Supported by Crohn’s & Colitis Foundation of America.
15
Pallotta, Nadia, Ernesto Tomei, Angelo Viscido, Emma Calabrese, Adriana Marcheggiano, Renzo Caprilli, and Enrico Corazziari. "Small Intestine Contrast Ultrasonography." Inflammatory Bowel Diseases 11, no. 2 (February 2005): 146–53. http://dx.doi.org/10.1097/00054725-200502000-00008.
Full text
16
Zhao, Yong, Yanni Feng, Ming Liu, Liang Chen, Qingshi Meng, Xiangfang Tang, Shukun Wang, et al. "Single-cell RNA sequencing analysis reveals alginate oligosaccharides preventing chemotherapy-induced mucositis." Mucosal Immunology 13, no. 3 (January 3, 2020): 437–48. http://dx.doi.org/10.1038/s41385-019-0248-z.
Full textAbstract:
AbstractWorldwide the incidence of cancer has been continuing increasing. Mucositis of the gastrointestinal tract is a common side effect in patients under chemotherapy. Anticancer drug busulfan, used for treating chronic myeloid leukemia especially in pediatric patients, causes mucositis of the gastrointestinal tract. Alginate oligosaccharides (AOS) are natural products with attractive pharmaceutical potentials. We aimed to investigate, at the single-cell level, AOS preventing small intestine mucositis induced by busulfan. We found that busulfan disturbed the endoplasmic reticulum and mitochondria of cells in the small intestine, damaged cell membranes especially cell junctions, and disrupted microvilli; all of which were rescued by AOS. Single-cell RNA sequencing analysis and functional enrichment analysis showed that AOS could recover small intestinal function. Deep analysis found that AOS improved the expression of transcriptional factors which explained AOS regulating gene expression to improve small intestine function. Further investigation in IPEC-J2 cells found that AOS acts its function through mannose receptor signaling pathway. Moreover, the improved blood metabolome confirmed small intestinal function was recovered by AOS. As a natural product with many advantages, AOS could be developed to assist in the recovery of intestinal functions in patients undergoing anticancer chemotherapy or other treatments.
17
Brandl, Katharina, George Plitas, Bernd Schnabl, Ronald P. DeMatteo, and Eric G. Pamer. "MyD88-mediated signals induce the bactericidal lectin RegIIIγ and protect mice against intestinal Listeria monocytogenes infection." Journal of Experimental Medicine 204, no. 8 (July 16, 2007): 1891–900. http://dx.doi.org/10.1084/jem.20070563.
Full textAbstract:
Listeria monocytogenes is a food-borne bacterial pathogen that causes systemic infection by traversing the intestinal mucosa. Although MyD88-mediated signals are essential for defense against systemic L. monocytogenes infection, the role of Toll-like receptor and MyD88 signaling in intestinal immunity against this pathogen has not been defined. We show that clearance of L. monocytogenes from the lumen of the distal small intestine is impaired in MyD88−/− mice. The distal ileum of wild-type (wt) mice expresses high levels of RegIIIγ, which is a bactericidal lectin that is secreted into the bowel lumen, whereas RegIIIγ expression in MyD88−/− mice is nearly undetectable. In vivo depletion of RegIIIγ from the small intestine of wt mice diminishes killing of luminal L. monocytogenes, whereas reconstitution of MyD88-deficient mice with recombinant RegIIIγ enhances intestinal bacterial clearance. Experiments with bone marrow chimeric mice reveal that MyD88-mediated signals in nonhematopoietic cells induce RegIIIγ expression in the small intestine, thereby enhancing bacterial killing. Our findings support a model of MyD88-mediated epithelial conditioning that protects the intestinal mucosa against bacterial invasion by inducing RegIIIγ.
18
De Oliveira, Marília Garcia, Rafaela Andreoni, Wesley Brandao, Beatriz Peixinho, Carolina Manganeli Polonio, Nagela Ghabdan Zanluqui, Lilian Oliveira, and Jean Pierre S. Peron. "The role of glutamate-NMDA-receptor in mice alpha beta T cells from intestinal mucosa." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 158.18. http://dx.doi.org/10.4049/jimmunol.204.supp.158.18.
Full textAbstract:
Abstract The intestinal mucosa consists of a simple layer of epithelial tissue and loose connective tissue called the lamina propria that is formed by several immune cells mainly T cells that play important roles in local tolerance to microorganisms of the microbiota and food antigens. In addition to mucosa the small and large intestines also present the submucosal and the muscular layers that present ganglionic enteric plexuses formed by networks of interconnection between autonomic neurons of the enteric nervous system. These neurons secrete various neurotransmitters including glutamate and their innervations reach the lamina propria. It is known that T cells have receptors for neurotransmitters even the ionotropic glutamate receptor NMDAR. Thus, the present study intends to evaluate the role of NMDAR in αβ T cells from intestinal mucosa. C57BL/6 Grin1f/f and CD4crexGrin1flox mice of both sexes were used at 8 weeks of age. CD4+ T cells, CD8+ T cells, γδT cells, dendritic cells and macrophages present in mesenteric lymph nodes and at intraepithelial compartment of small intestine were evaluated. We found that CD8+ T cells were decreased and γδT cells were increased in mesenteric lymph nodes of CD4crexGrin1flox mice in comparison to the control group. Thus, intraepithelial CD4+ T cells and macrophages were increased, but intraepithelial CD8+ T cells were decreased in small intestine of CD4crexGrin1flox mice compared to the control group. Our preliminary results shows that the absence of NMDAR exclusively in αβ T cells alters the percentage of immune cells present both in mesenteric lymph nodes and intraepithelial compartment of small intestine suggesting a modulation by glutamate. New evaluations are still in progress to better understand that.
19
Camerini, Victoria, Beate C. Sydora23, Richard Aranda, Chris Nguyen, Colin MacLean, William H. McBride, and Mitchell Kronenberg. "Generation of Intestinal Mucosal Lymphocytes in SCID Mice Reconstituted with Mature, Thymus-Derived T Cells." Journal of Immunology 160, no. 6 (March 15, 1998): 2608–18. http://dx.doi.org/10.4049/jimmunol.160.6.2608.
Full textAbstract:
Abstract Transfer of peripheral lymph node lymphocytes to SCID mice leads to the long term establishment of mucosal T lymphocytes within the epithelium and lamina propria of the small and large intestines. Analysis of engrafted intraepithelial lymphocytes (IEL) showed that they had acquired a surface phenotype that in several respects is typical of IEL. In addition, the functional profile of engrafted IEL derived from lymph node T cells was similar to that of normal IEL; as the donor-derived T cells exhibited a strong cytolytic activity, a poor proliferative response to mitogenic stimuli, and a tendency to home and expand specifically in the intestine upon transfer to secondary SCID recipients. Optimal engraftment of intestinal T cells required bacterial flora, as the number of lymphocytes was greatly reduced in SCID recipients with a reduced flora. These results demonstrate that mature, thymus-derived T cells can migrate to the intestine and become functionally specialized to the intestinal milieu. The acquisition of phenotypic markers characteristic of the intestinal microenvironment by engrafted cells suggests that T cell migration of lymphocytes to the SCID intestine is not aberrant, but it may reflect processes that are ongoing in immunocompetent mice. Furthermore, these data suggest that the homing and/or expansion of typical, thymus-derived T cells in the intestine may be driven by luminal Ags such as those derived from bacterial flora.
20
Fujiwara, Daisuke, Bo Wei, and Jonathan Braun. "Role of small intestinal intraepithelial CD11c+ CD8+ T cells in mucosal immunoregulation (39.36)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 39.36. http://dx.doi.org/10.4049/jimmunol.182.supp.39.36.
Full textAbstract:
Abstract The chronic intestinal inflammation tends to occur in the large intestine (LI) rather than in the small intestine (SI) partly due to the relative abundant microbial colonization in LI. However, intestinal intraepithelial T lymphocytes (IEL) in the large intestine are also distinguished from these in the small intestine. In this study, we investigated the possibility that the phenotypic difference of immune populations in two immune compartments might represent their differed immunoregulatory functions for regional control of mucosal inflammation. We observed that in total IELs population, about 36-40% cells in SI and 12-15% cells in LI are CD11c+ and CD3+ double positive cells. The majority of these CD11c+ CD3+T cells were CD8 positive expressing either TCRαβ or γδ. Their T cell lineage was defined by TCR expression and generation of IEL CD11c+ T cells after transfer of CD45.1 splenic T cell into RAG2-/- mice. Compared with CD11c- CD3+ T cells, CD11c+ CD3+ T cells produced significantly lower levels of pro-inflammatory cytokines including TNF-α?and IFN-γ. In mouse model of Gαi2 KO T cells induced colitis, 2.5×105 of SI CD11c+ CD3+ T cells suppressed pro-inflammatory cytokine-producing CD4 T cells at the mucosal sites and protected mice from colitis development. In contrast, LI CD11c+ CD3+ T cells or SI CD11c- CD3+ T cells were ineffective in colitis protection. Taken together, these findings indicate that SI CD11c+ CD8+ T cells might be a functional T cell population that plays an immunoregulatory role in control of pro-inflammatory CD4+ T cells and maintenance of mucosal homeostasis in the intestine.
21
Huang, Hsin-I., Nourhan Youssef, Mark Jewell, Min-Nung Huang, and Gianna Hammer. "Th17 immunity in the colon is controlled by two novel subsets of colon-specific mononuclear phagocytes." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 158.3. http://dx.doi.org/10.4049/jimmunol.204.supp.158.3.
Full textAbstract:
Abstract Immune responses in the intestine are coordinated by specialized populations of mononuclear phagocytes. Although the functions of intestine-resident mononuclear phagocytes and the different cell subsets that constitute these populations are thought uniform across the entire intestine, it is clear that the anatomy, microbes, and immunological demands are distinct for small and large intestine. Whether these distinctions also include organ-specific mononuclear phagocyte populations, or that these have organ-specific roles in immunity are unknown. Here we identify two novel subsets of colon-specific mononuclear phagocytes, a dendritic cell (DC) subset and a macrophage subset, both of which are exclusive to the colon and are not found in small intestine. These colon-specific DCs and macrophages co-expressed CD14 and CD24, markers which are generally singularly expressed by intestinal DCs and macrophages and commonly used to distinguish between these two cell types. Colon-specific CD14+CD24+ DCs and macrophages failed to express macrophage markers CX3CR1, F4/80, CD64 and CD88, and surprisingly, both the DC and macrophage subset were dependent on the transcription factor IRF4. We further find that colon and small intestine have distinct antigen presenting cell (APC) requirements for Th17 immunity and that while colon-specific CD14+CD24+ APCs were essential for Th17 immunity in the colon, this role in small intestine was mediated by different APC subsets. Our findings reveal unappreciated organ-specific diversity of intestine-resident mononuclear phagocytes and organ-specific requirements for Th17 immunity.
22
Nagamine, Claude M., Jane J. Sohn, Barry H. Rickman, Arlin B. Rogers, James G. Fox, and David B. Schauer. "Helicobacter hepaticus Infection Promotes Colon Tumorigenesis in the BALB/c-Rag2−/−ApcMin/+ Mouse." Infection and Immunity 76, no. 6 (April 14, 2008): 2758–66. http://dx.doi.org/10.1128/iai.01604-07.
Full textAbstract:
ABSTRACT Adenomatous polyposis coli (APC) mutations are linked to human and mouse colorectal cancers. The Apc multiple intestinal neoplasia (Min) mouse mutation causes adenomas to develop throughout the small and large intestines. The BALB-Min (C.B6-Apc Min/+) congenic strain was generated by backcrossing into BALB/c the Apc Min allele from C57BL/6J-Apc Min/+ mice. BALB-Min mice have a low tumor multiplicity (27.4 small intestine tumors/mouse) and a relatively long life span (>1 year) that makes them amenable to long-term studies. To investigate the interplay of the adaptive immune system and intestinal tumorigenesis, the immunodeficient compound mutant strain BALB-RagMin (C.Cg-Rag2 −/− Apc Min/+) was generated. BALB-RagMin mice had a significant increase in tumors in the small, but not large, intestine relative to their BALB-Min counterparts (43.0 versus 24.0 tumors/mouse, respectively). The results suggest that the adaptive immune system plays a role in either the elimination or the equilibrium phase of cancer immunoediting in the small intestine in this model. We investigated the effect of the enterohepatic bacterial pathogen Helicobacter hepaticus on liver and intestine tumorigenesis in BALB-RagMin mice. H. hepaticus-infected BALB-RagMin mice developed moderate hepatitis, moderate typhlitis, and mild colitis. There were no differences in small intestine and cecal tumor multiplicity, regionality, or size relative to that in uninfected mice. However, H. hepaticus-infected BALB-RagMin mice had a significant increase in colon tumor incidence relative to uninfected BALB-RagMin mice (23.5% versus 1.7%, respectively). The data suggest that H. hepaticus, which is present in many research colonies, promotes colon tumorigenesis in the BALB-RagMin mouse and that it has the potential to confound colon tumorigenesis studies.
23
Taylor, Rebekah, Jennifer Kleponis, Russia Tatum, and Fernando Terrero. "Absence of organized lymphoid tissues in the intestine of the freshwater fish, C. commersonii (VET2P.1042)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 207.14. http://dx.doi.org/10.4049/jimmunol.192.supp.207.14.
Full textAbstract:
Abstract Microscopic organized lymphoid tissues in the small intestine, such as cryptopatches (CP) and isolated lymphoid follicles (ILF), have been well characterized in the laboratory mouse. Descriptions of these structures have also been reported in rat and human, but the presence or absence of CP and ILF in other animals has not been explored. Given the evolutionary development of the adaptive immune system beginning in jawed fish, we hypothesized that CP and ILF would be present in the intestines of fish. We examined the intestines of 10 wild-caught Catostomus commersonii, a bottom-feeding freshwater fish found in local streams in Western Maryland and throughout the United States. The intestines of these fish were opened longitudinally and arranged in flattened layers for horizontal sectioning. Samples of mouse small intestine were prepared simultaneously as a positive control. After quick-freezing and sectioning, the tissue was stained with hematoxylin and eosin. Interestingly, a complete absence of organized lymphoid tissue was noted, suggesting that CP and ILF, in addition to the well-known Peyer’s patches, are limited to higher-order animals and potentially only mammals. Plans to study other fish species, especially carnivorous varieties (since the composition of the intestinal immune system can change in response to diet) are currently underway to further support this finding.
24
Kantak, A. G., R. M. Goldblum, M. Z. Schwartz, S. Rajaraman, C. T. Ladoulis, and A. S. Goldman. "Fetal intestinal transplants in syngeneic rats: a developmental model of intestinal immunity." Journal of Immunology 138, no. 10 (May 15, 1987): 3191–96. http://dx.doi.org/10.4049/jimmunol.138.10.3191.
Full textAbstract:
Abstract We conducted a longitudinal study of the development of lymphoid tissue in fetal small intestine transplanted to a subcutaneous site in adult syngeneic Fischer strain rats. Fetal jejunoileal segments obtained between 18 and 21 days of gestation were transplanted to a dorsal subcutaneous site on syngeneic adult rats. Three weeks later, intestinal segments greater than 2.5 cm in length were found in 70% of recipients. Each week for 6 wk post-transplantation, a full-thickness biopsy was obtained for histologic and immunohistologic examination. At the time of transplantation, fetal rat intestine did not display Peyer's patches, intraepithelial lymphocytes, lymphoid follicles, or IgA-containing plasma cells. These lymphoid structures reached adult levels by 4 wk after transplantation, and the sequence of development of the lymphoid structures in the transplants appeared to match the postnatal development of normal small intestine. After immunizing the in situ intestine or the transplanted fetal intestine with cholera toxin, the number of cells producing specific antibodies to the immunogen increased significantly in intestinal transplants and in situ intestine. In contrast, few if any cells synthesizing antibodies to cholera toxin developed in the transplants after i.p. immunization. This study suggests that fetal intestinal transplants behave as part of the mucosal immune system. This model may provide useful approaches to studying the development of mucosal immunity.
25
Pabst, Oliver, Lars Ohl, Meike Wendland, Marc-André Wurbel, Elisabeth Kremmer, Bernard Malissen, and Reinhold Förster. "Chemokine Receptor CCR9 Contributes to the Localization of Plasma Cells to the Small Intestine." Journal of Experimental Medicine 199, no. 3 (January 26, 2004): 411–16. http://dx.doi.org/10.1084/jem.20030996.
Full textAbstract:
Humoral immunity in the gut-associated lymphoid tissue is characterized by the production of immunoglobulin A (IgA) by antibody-secreting plasma cells (PCs) in the lamina propria. The chemokine CCL25 is expressed by intestinal epithelial cells and is capable of inducing chemotaxis of IgA+ PCs in vitro. Using a newly generated monoclonal antibody against murine CCR9, we show that IgA+ PCs express high levels of CCR9 in the mesenteric lymph node (MLN) and Peyer's patches (PPs), but down-regulate CCR9 once they are located in the small intestine. In CCR9-deficient mice, IgA+ PCs are substantially reduced in number in the lamina propria of the small intestine. In adoptive transfer experiments, CCR9-deficient IgA+ PCs show reduced migration into the small intestine compared with wild-type controls. Furthermore, CCR9 mutants fail to mount a regular IgA response to an orally administered antigen, although the architecture and cell type composition of PPs and MLN are unaffected and are functional for the generation of IgA PCs. These findings provide profound in vivo evidence that CCL25/CCR9 guides PCs into the small intestine.
26
Minton, Kirsty. "ILC3s take control in small intestine." Nature Reviews Immunology 19, no. 6 (April 12, 2019): 353. http://dx.doi.org/10.1038/s41577-019-0166-z.
Full text
27
Schulz, Olga, and Oliver Pabst. "Antigen sampling in the small intestine." Trends in Immunology 34, no. 4 (April 2013): 155–61. http://dx.doi.org/10.1016/j.it.2012.09.006.
Full text
28
Rivera-Nieves, Jesús, Tracy L. Burcin, Timothy S. Olson, Margaret A. Morris, Marcia McDuffie, Fabio Cominelli, and Klaus Ley. "Critical role of endothelial P-selectin glycoprotein ligand 1 in chronic murine ileitis." Journal of Experimental Medicine 203, no. 4 (March 27, 2006): 907–17. http://dx.doi.org/10.1084/jem.20052530.
Full textAbstract:
L-selectin ligands might be relevant for inflammatory cell trafficking into the small intestine in a spontaneous model of chronic ileitis (i.e., SAMP1/YitFc mice). Immunoblockade of peripheral node addressin or mucosal addressin cell adhesion molecule 1 failed to ameliorate ileitis, whereas P-selectin glycoprotein ligand 1 (PSGL-1) neutralization attenuated both the adoptively transferred and spontaneous disease. PSGL-1 was detected in venules of mesenteric lymph node and small intestine by immunohistochemistry and confirmed by real-time reverse transcription polymerase chain reaction and flow cytometry. In addition, reconstitution of wild-type mice with PSGL-1−/− bone marrow demonstrated that PSGL-1 messenger RNA and PSGL-1 protein expression remained on endothelium, localized within mesenteric lymph node and small intestine. Endothelial PSGL-1 bound P-selectin–IgG and its blockade or genetic deletion altered the recruitment of lymphocytes to the small intestine, as revealed by intravital microscopy and homing studies. Endothelial expression of PSGL-1 adds a new dimension to the various cellular interactions involved in small intestinal recruitment. Thus, the multiple roles of PSGL-1 may explain why targeting this single adhesion molecule results in attenuation of chronic murine ileitis, a disease previously resistant to antiadhesion molecule strategies.
29
MacDonald, T. T., and J. Spencer. "Evidence that activated mucosal T cells play a role in the pathogenesis of enteropathy in human small intestine." Journal of Experimental Medicine 167, no. 4 (April 1, 1988): 1341–49. http://dx.doi.org/10.1084/jem.167.4.1341.
Full textAbstract:
T cells in explants of human fetal small intestine in organ culture were stimulated in situ with PWM or anti-CD3 antibody to test the hypothesis that activated T cells produce enteropathy in human small intestine. T cell activation was measured by the appearance of CD25+ cells in the lamina propria of the explants and IL-2 production into the organ culture supernatant. We have previously shown that the number of T cells in human fetal gut increased between 14 and 22 wk gestation. Accordingly, after the addition of PWM to cultured explants of fetal intestine the number of CD25+ cells in the lamina propria and the amounts of IL-2 secreted into the organ culture supernatant increased with the age of the explanted tissue. The addition of PWM also produced an age-related enteropathy, most noticeably crypt epithelial cell hyperplasia and villous atrophy, with relatively minor changes in 14-17-wk-old intestine but severe tissue damage in 18-22-wk-old fetal intestine. These enteropathic effects were also produced when mucosal T cells were activated with anti-CD3 mAb. Cyclosporin A completely inhibited the PWM-induced development of CD25+ cells and related tissue damage. These experiments show that activated T cells in human small intestine produce enteropathy. The model provides a new system with which to dissect the mechanisms of T cell-mediated intestinal damage.
30
Norkina, Oxana, Tim G. Burnett, and Robert C. De Lisle. "Bacterial Overgrowth in the Cystic Fibrosis Transmembrane Conductance Regulator Null Mouse Small Intestine." Infection and Immunity 72, no. 10 (October 2004): 6040–49. http://dx.doi.org/10.1128/iai.72.10.6040-6049.2004.
Full textAbstract:
ABSTRACT We recently reported the inflammation of the cystic fibrosis (CF) mouse small intestine, and we hypothesized bacterial overgrowth as a possible cause. Quantitative PCR of bacterial 16S genomic DNA in the CF mouse small intestine revealed an increase of greater than 40-fold compared to controls. Sequencing of 16S PCR products and Gram staining showed that the majority of bacteria in the CF mouse intestine were gram negative. Bacteria were observed to colonize the mucus that accumulates in the intestinal lumen of mice with CF. Impaired Paneth cell defenses were suggested by observation of partially dispersed Paneth granules in the mucus plugs of CF mouse intestinal crypts, and this mucus was strongly immunoreactive for Paneth cell bactericidal products. The role of bacterial overgrowth in intestinal inflammation in CF was tested by treating mice with oral antibiotics (ciprofloxacin and metronidazole) for 3 weeks, which reduced bacterial load in the CF mouse small intestine over 400-fold. Antibiotic treatment decreased the expression of the inflammation-related genes mast cell protease 2, leucine-rich α2 glycoprotein/leucine-rich high endothelial venule glycoprotein, suppressor of cytokine signaling 3, hematopoietic cell transcript 1, and resistin-like molecule β/found in inflammatory zone 2, all of which were no longer expressed at levels significantly different from control levels. The reduction of intestinal bacteria also significantly improved the growth of CF mice but had no effect on the growth of wild-type mice. These data suggest that bacterial overgrowth in the CF mouse small intestine has a role in inflammation and contributes to the failure to thrive in this mouse model of CF.
31
Cho, Hyeseon, Rosanne Spolski, Byunghyun Kang, Warren J. Leonard, and Brian L. Kelsall. "Microbiota-dependent IL-21 signaling regulates intestinal immune cell homeostasis and immunopathology to infection." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 200.7. http://dx.doi.org/10.4049/jimmunol.198.supp.200.7.
Full textAbstract:
Abstract Despite studies indicating a role for IL-21 in intestinal inflammation, how it precisely affects intestinal homeostasis and immunity to infection is not yet clear. In this study, we report a potent effect of commensal microbiota on the phenotypic manifestations of IL-21 receptor deficiency. IL-21 is expressed highly by CD4 T cells of Peyer’s patches (PPs) and small intestine lamina propria (LP) and strongly induced by co-housing with SFB-positive mice. Mice deficient in IL-21 receptor exhibit reduced numbers of GC B cells, B cell expression of AID, and IgA+ B cell populations in PPs, consistent with the known roles for IL-21 in B cell function. Consequently, IL-21R KO mice show a significant reduction in IgA+ plasmablasts and plasma cells in the small intestine LP. Interestingly, microbiota-dependent increases in RORgt+ T cells and Treg cells are observed in the small intestine of IL21-R KO mice. Neither the Th1 nor RORgt+ ILC populations are altered in the KO mice intestine compared to WT mice. Demonstrating a critical role of IL-21 signaling in immunopathology during Citrobacter rodentium infection, IL-21 receptor deficiency leads to strikingly reduced tissue pathology without affecting bacterial clearance. This reduced immunopathology likely results from dampened production of IFNg, IL-12, and IL-1b that promote severe immunopathology/lethality. Taken together, we demonstrate the regional and pleotropic effects of IL-21 signaling that fine-tunes intestinal mucosal immunity in a microbiota-dependent manner, which has significant implication for anti-IL-21 therapy to treat inflammatory bowel disease.
32
Umesaki, Yoshinori, Hiromi Setoyama, Satoshi Matsumoto, Akemi Imaoka, and Kikuji Itoh. "Differential Roles of Segmented Filamentous Bacteria and Clostridia in Development of the Intestinal Immune System." Infection and Immunity 67, no. 7 (July 1, 1999): 3504–11. http://dx.doi.org/10.1128/iai.67.7.3504-3511.1999.
Full textAbstract:
ABSTRACT The presence of microflora in the digestive tract promotes the development of the intestinal immune system. In this study, to evaluate the roles of two types of indigenous microbe, segmented filamentous bacteria (SFB) and clostridia, whose habitats are the small and large intestines, respectively, in this immunological development, we analyzed three kinds of gnotobiotic mice contaminated with SFB, clostridia, and both SFB and clostridia, respectively, in comparison with germfree (GF) or conventionalized (Cvd) mice associated with specific-pathogen-free flora. In the small intestine, the number of αβ T-cell receptor-bearing intraepithelial lymphocytes (αβIEL) increased in SFB-associated mice (SFB-mice) but not in clostridium-associated mice (Clost-mice). There was no great difference in Vβ usage among GF mice, Cvd mice, and these gnotobiotic mice, although the association with SFB decreased the proportion of Vβ6+ cells in CD8β− subsets to some extent, compared to that in GF mice. The expression of major histocompatibility complex class II molecules on the epithelial cells was observed in SFB-mice but not in Clost-mice. On the other hand, in the large intestine, the ratio of the number of CD4−CD8+ cells to that of CD4+ CD8−cells in αβIEL increased in Clost-mice but not in SFB-mice. On association with both SFB and clostridia, the numbers and phenotypes of IEL in the small and large intestines changed to become similar to those in Cvd mice. In particular, the ratio of the number of CD8αβ+ cells to that of CD8αα+ cells in αβIEL, unusually elevated in the small intestines of SFB-mice, decreased to the level in Cvd mice on contamination with both SFB and clostridia. The number of immunoglobulin A (IgA)-producing cells in the lamina propria was more elevated in SFB-mice than in Clost-mice, not only in the ileum but also in the colon. The number of IgA-producing cells in the colons of Clost-mice was a little increased compared to that in GF mice. Taken together, SFB and clostridia promoted the development of both IEL and IgA-producing cells in the small intestine and that of only IEL in the large intestine, respectively, suggesting the occurrence of compartmentalization of the immunological responses to the indigenous bacteria between the small and large intestines.
33
Ahn, Ji-Seon, Enkhchimeg Lkhagva, Sunjun Jung, Hyeon-Jin Kim, Hea-Jong Chung, and Seong-Tshool Hong. "Fecal Microbiome Does Not Represent Whole Gut Microbiome." Cellular Microbiology 2023 (January 17, 2023): 1–14. http://dx.doi.org/10.1155/2023/6868417.
Full textAbstract:
The current gut microbiome research relies on the fecal microbiome under the assumption that the fecal microbiome represents the microbiome of the entire gastrointestinal (GI) tract. However, there have been growing concerns about using feces as a proxy to study the gut microbiome. Here, we comprehensively analyzed the composition of microbiome and metabolites in the feces and at 14 different locations of GI tracts of genetically homogenous sibling pigs to evaluate the validity of using feces as a proxy to the whole gut microbiome. The composition of intestinal microbes constituting the gut microbiome at each intestinal content and feces and their metabolic compositions were thoroughly investigated through metagenome sequencing and an ultraperformance LC-MS/MS, respectively. The fluctuation in the composition of the microbiome in the stomach and the small intestine became stabilized from the large intestine to feces and was able to be categorized into 3 groups. The taxonomic α-diversities measured by ACE (abundance-based coverage estimator) richness and Shannon diversity indicated that the microbiome in the large intestine was much more diverse than those of the small intestine and feces. The highly independent intestinal microbes in the stomach and the small intestine became flourished in the large intestine and converged into a community with tightly connected networks. β-Diversity analyses by NMDS plots, PCA, and unsupervised hierarchical clustering all showed that the diversities of microbiome compositions were lowest in feces while highest in the large intestine. In accordance with fluctuation of the composition of gut microbiome along with the GI tract, the metabolic composition also completely differed in a location-specific manner along with the GI tract. Comparative analysis of the fecal microbiome and metabolites with those of the whole GI tract indicated that fecal microbiome is insufficient to represent the whole gut microbiome.
34
Bujko, Anna, Nader Atlasy, Ole J. B. Landsverk, Lisa Richter, Sheraz Yaqub, Rune Horneland, Ole Øyen, et al. "Transcriptional and functional profiling defines human small intestinal macrophage subsets." Journal of Experimental Medicine 215, no. 2 (December 22, 2017): 441–58. http://dx.doi.org/10.1084/jem.20170057.
Full textAbstract:
Macrophages (Mfs) are instrumental in maintaining immune homeostasis in the intestine, yet studies on the origin and heterogeneity of human intestinal Mfs are scarce. Here, we identified four distinct Mf subpopulations in human small intestine (SI). Assessment of their turnover in duodenal transplants revealed that all Mf subsets were completely replaced over time; Mf1 and Mf2, phenotypically similar to peripheral blood monocytes (PBMos), were largely replaced within 3 wk, whereas two subsets with features of mature Mfs, Mf3 and Mf4, exhibited significantly slower replacement. Mf3 and Mf4 localized differently in SI; Mf3 formed a dense network in mucosal lamina propria, whereas Mf4 was enriched in submucosa. Transcriptional analysis showed that all Mf subsets were markedly distinct from PBMos and dendritic cells. Compared with PBMos, Mf subpopulations showed reduced responsiveness to proinflammatory stimuli but were proficient at endocytosis of particulate and soluble material. These data provide a comprehensive analysis of human SI Mf population and suggest a precursor-progeny relationship with PBMos.
35
Gurish, Michael F., Hong Tao, J. Pablo Abonia, Anu Arya, Daniel S. Friend, Christina M. Parker, and K. Frank Austen. "Intestinal Mast Cell Progenitors Require CD49dβ7 (α4β7 Integrin) for Tissue-specific Homing." Journal of Experimental Medicine 194, no. 9 (October 29, 2001): 1243–52. http://dx.doi.org/10.1084/jem.194.9.1243.
Full textAbstract:
Mast cells (MCs) are centrally important in allergic inflammation of the airways, as well as in the intestinal immune response to helminth infection. A single lineage of bone marrow (BM)-derived progenitors emigrates from the circulation and matures into phenotypically distinct MCs in different tissues. Because the mechanisms of MC progenitor (MCp) homing to peripheral tissues have not been evaluated, we used limiting dilution analysis to measure the concentration of MCp in various tissues of mice deficient for candidate homing molecules. MCp were almost completely absent in the small intestine but were present in the lung, spleen, BM, and large intestine of β7 integrin-deficient mice (on the C57BL/6 background), indicating that a β7 integrin is critical for homing of these cells to the small intestine. MCp concentrations were not altered in the tissues of mice deficient in the αE integrin (CD103), the β2 integrin (CD18), or the recombination activating gene (RAG)-2 gene either alone or in combination with the interleukin (IL)-receptor common γ chain. Therefore, it is the α4β7 integrin and not the αEβ7 integrin that is critical, and lymphocytes and natural killer cells play no role in directing MCp migration under basal conditions. When MCp in BALB/c mice were eliminated with sublethal doses of γ-radiation and then reconstituted with syngeneic BM, the administration of anti-α4β7 integrin, anti-α4 integrin, anti-β7 integrin, or anti–MAdCAM-1 monoclonal antibodies (mAbs) blocked the recovery of MCp in the small intestine. The blocking mAbs could be administered as late as 4 d after BM reconstitution with optimal inhibition, implying that the MCp must arise first in the BM, circulate in the vasculature, and then translocate into the intestine. Inasmuch as MCp are preserved in the lungs of β7 integrin-deficient and anti-α4β7 integrin-treated mice but not in the small intestine, α4β7 integrin is critical for tissue specific extravasation for localization of MCp in the small intestine, but not the lungs.
36
Oyesola, Oyebola Oluwakemi, Lauren M. Webb, Sabrina Solouki, Duc Pham, Pamela Campioli, Rebecca Cubitt, and Elia D. Tait Wojno. "The prostaglandin D2 receptor CRTH2 suppresses epithelial cell responses during intestinal helminth infection." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 65.1. http://dx.doi.org/10.4049/jimmunol.198.supp.65.1.
Full textAbstract:
Abstract Type 2 inflammation is required for expulsion of intestinal helminth parasites and is characterized by immune cell activation, type 2 cytokine production, and increased mucin production by epithelial goblet cells. Previous studies show that the prostaglandin D2 (PGD2) receptor chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2) promotes type 2 inflammation in the lung via effects on immune cells, but how CRTH2 influences helminth-induced type 2 inflammation in the intestine was unclear. Here we show that CRTH2-deficient mice cleared infection with the mouse-adapted helminth parasite Nippostrongylus brasiliensis more efficiently and had increased numbers of mucin-producing goblet cells in the small intestine post-infection compared to wild type mice, despite similar levels of worm establishment. These data suggest that CRTH2 restrains goblet cell responses during intestinal helminth infection, in contrast to its pro-inflammatory role in the lung. Consistent with this idea, bone marrow-chimeric mice in which only non-hematopoietic cells lacked CRTH2 also cleared parasites more efficiently than chimeric wild type mice and had increased numbers of small intestinal goblet cells. In addition, murine small intestinal organoids that were stimulated with type 2 cytokines downregulated expression of goblet cell-associated genes following culture with PGD2. Taken together, these data suggest that the PGD2-CRTH2 pathway suppresses epithelial goblet cell responses following helminth-induced type 2 inflammation in the intestine. These findings may inform the development and use of drugs that inhibit this pathway during intestinal type 2 inflammatory disease, such as food allergy.
37
Wai, Lu-En, Mouer Wang, Karine Piard-Ruster, Olivia Martinez, and Sheri Krams. "Allograft survival is prolonged in the absence of NKG2D (169.19)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 169.19. http://dx.doi.org/10.4049/jimmunol.186.supp.169.19.
Full textAbstract:
Abstract NKG2D is expressed by Natural Killer (NK cells) and subsets of T cells. On NK cells, NKG2D functions as a stimulatory receptor that induces effector functions. We have demonstrated increased expression of NKG2D ligands on rejecting grafts and enhanced infiltration of NKG2D-expressing cells in allografts during rejection. To further examine the role of NKG2D in graft survival we utilized Klrk1 mice that are deficient for NKG2D as recipients of cardiac or small intestine allografts. Groups (n=4-6) of C57BL/6 (H-2b) or NKG2D deficient Klrk1 mice (H-2b) received heterotopic donor hearts or vascularized, orthotopic small intestine grafts from BALB/c (H-2d) or BALB/c x C57BL/6 F1 mice (H-2d/b). Some groups of mice also received 200μg (heart) or 500μg (intestine) anti-CD40L mAb (MR1) at transplant. Cardiac allograft survival was similar in wild-type and Klrk1 mice although intestinal allograft survival was prolonged in Klrk1 mice. Treatment with MR1 prolonged cardiac allograft survival that was further enhanced in the absence of NKG2D. Treatment with MR1 did not prolong survival of intestine allografts in wild-type recipients. Quite dramatically, however, treatment with MR1, significantly (p=0.007) prolonged intestinal allograft survival in Klrk1 mice. Prolongation of intestinal graft survival in the absence of NKG2D and CD40-CD40L interactions suggest that the addition of therapeutics to block NKG2D has great potential for improving costimulation blockade based therapies
38
Morales, Victor M., Andreas Christ, Suzanne M. Watt, Hyun S. Kim, Kevin W. Johnson, Nalan Utku, Ana M. Texieira, et al. "Regulation of Human Intestinal Intraepithelial Lymphocyte Cytolytic Function by Biliary Glycoprotein (CD66a)." Journal of Immunology 163, no. 3 (August 1, 1999): 1363–70. http://dx.doi.org/10.4049/jimmunol.163.3.1363.
Full textAbstract:
Abstract Human small intestinal intraepithelial lymphocytes (iIEL) are a unique population of CD8αβ+ TCR-αβ+ but CD28− T lymphocytes that may function in intestinal epithelial cell immunosurveillance. In an attempt to define novel cell surface molecules involved in iIEL function, we raised several mAbs against activated iIELs derived from the small intestine that recognized an Ag on activated, but not resting, iIELs. Using expression cloning and binding studies with Fc fusion proteins and transfectants, the cognate Ag of these mAbs was identified as the N domain of biliary glycoprotein (CD66a), a carcinoembryonic Ag-related molecule that contains an immune receptor tyrosine-based inhibitory motif. Functionally, these mAbs inhibited the anti-CD3-directed and lymphokine-activated killer activity of the P815 cell line by iIELs derived from the human small intestine. These studies indicate that the expression of biliary glycoprotein on activated human iIELs and, potentially, other mucosal T lymphocytes is involved in the down-regulation of cytolytic function.
39
Zheng, Mingzhu, Kairui Mao, Dan Li, Difeng Fang, Jun Lyu, and Jinfang (Jeff) Zhu. "B cell recruitment to the intestine critically depends on GATA3- and RORgt-mediated development of NKp46 negative innate lymphoid cells." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 188.10. http://dx.doi.org/10.4049/jimmunol.202.supp.188.10.
Full textAbstract:
Abstract The isolated lymphoid follicles (ILFs) enrich for B cells, most of which are conventional B cells, however, how they are recruited into and remain in intestine is not fully understood. Here, we show that in the small intestine lamina propria (siLP) of the Gata3f/f-VavCre mouse strain, in which no T cells and very few innate lymphoid cells (ILCs) are present, B cells were also largely absent, despite B cells were normal in number in the spleen of these mice. Mixed bone marrow chimera experiments showed that Gata3-deficient B cells were able to migrate to the siLP. Normal intestinal B cells were found in Tcra−/− mice excluding the possibility of T cell contribution to B cell recruitment. Bone marrow reconstitution of various donors into Gata3f/f-VavCre mice indicated that ILCs were involved in B cell migrating into small intestine LP. Further immunofluorescent analyses using RorcGFP/GFPand Gata3f/f-Rorc-Cre mice implicated that deficiency in NKp46 negative ILC3s, presumably the lymphoid tissue inducers, was responsible for impaired B cell recruitment. In summary, our findings suggest that NKp46 negative ILC3-mediated formation of tertiary lymphoid structures such as ILFs is required for B cell recruitment and/or retention in the small intestine.
40
Kunkel, Eric J., James J. Campbell, Guttorm Haraldsen, Junliang Pan, Judie Boisvert, Arthur I. Roberts, Ellen C. Ebert, et al. "Lymphocyte Cc Chemokine Receptor 9 and Epithelial Thymus-Expressed Chemokine (Teck) Expression Distinguish the Small Intestinal Immune Compartment." Journal of Experimental Medicine 192, no. 5 (September 5, 2000): 761–68. http://dx.doi.org/10.1084/jem.192.5.761.
Full textAbstract:
The immune system has evolved specialized cellular and molecular mechanisms for targeting and regulating immune responses at epithelial surfaces. Here we show that small intestinal intraepithelial lymphocytes and lamina propria lymphocytes migrate to thymus-expressed chemokine (TECK). This attraction is mediated by CC chemokine receptor (CCR)9, a chemoattractant receptor expressed at high levels by essentially all CD4+ and CD8+ T lymphocytes in the small intestine. Only a small subset of lymphocytes in the colon are CCR9+, and lymphocytes from other tissues including tonsils, lung, inflamed liver, normal or inflamed skin, inflamed synovium and synovial fluid, breast milk, and seminal fluid are universally CCR9−. TECK expression is also restricted to the small intestine: immunohistochemistry reveals that intense anti-TECK reactivity characterizes crypt epithelium in the jejunum and ileum, but not in other epithelia of the digestive tract (including stomach and colon), skin, lung, or salivary gland. These results imply a restricted role for lymphocyte CCR9 and its ligand TECK in the small intestine, and provide the first evidence for distinctive mechanisms of lymphocyte recruitment that may permit functional specialization of immune responses in different segments of the gastrointestinal tract. Selective expression of chemokines by differentiated epithelium may represent an important mechanism for targeting and specialization of immune responses.
41
Kunisawa, Jun, Yosuke Kurashima, Morio Higuchi, Masashi Gohda, Izumi Ishikawa, Ikuko Ogahara, Namju Kim, Miki Shimizu, and Hiroshi Kiyono. "Sphingosine 1-phosphate dependence in the regulation of lymphocyte trafficking to the gut epithelium." Journal of Experimental Medicine 204, no. 10 (September 17, 2007): 2335–48. http://dx.doi.org/10.1084/jem.20062446.
Full textAbstract:
It is well established that intraepithelial T lymphocytes (IELs) are derived from conventional single-positive (SP) thymocytes, as well as unconventional double-negative (DN) thymocytes and CD103+CD8αβ recent thymic emigrants (RTEs). We show that IELs can be divided into two groups according to their dependency on sphingosine 1-phosphate (S1P) for trafficking into the intestines. CD4 or CD8αβ naive lymphocytes originating from SP thymocytes express high levels of type 1 S1P receptor (S1P1), and their preferential migration into the large intestine is regulated by S1P. In contrast, RTEs migrate exclusively into the small intestine, whereas DN thymic IEL precursors expressing either TCRαβ or TCRγδ migrate into both the small and large intestines. S1P does not play a role in the migration pathways of these unconventional thymic IEL precursors. Thus, down-regulation of S1P1 expression or disruption of the S1P gradient halted conventional CD4 or CD8αβ IEL trafficking into the intestines, but did not affect the trafficking of unconventional thymic IEL precursors. These data are the first to demonstrate that a lipid-mediated system discriminates IELs originating from conventional and unconventional thymic precursors.
42
Holtmeier, W., T. Witthöft, A. Hennemann, H. S. Winter, and M. F. Kagnoff. "The TCR-delta repertoire in human intestine undergoes characteristic changes during fetal to adult development." Journal of Immunology 158, no. 12 (June 15, 1997): 5632–41. http://dx.doi.org/10.4049/jimmunol.158.12.5632.
Full textAbstract:
Abstract The TCR-delta repertoire in adult human intestine is oligoclonal and unique in each individual. In the present study, changes in the junctional regions of TCR-delta transcripts in human intestine that occur during development from fetal to adult life were used to characterize fundamental changes in the TCR-delta repertoire in the human intestinal tract during ontogeny. At mid-gestation, the fetal repertoire was polyclonal, but limited, in its junctional diversity by the relative lack of N region nucleotide additions and by the frequent formation of coding region joins at regions of short sequence homology. In addition, identical TCRDV2 transcripts that resemble canonical TCR-delta sequences in mice were present in the intestine of different fetuses. In the early period after birth, the intestinal TCR-delta repertoire was polyclonal, and more diverse than the fetal repertoire, with junctional regions that contained extensive N nucleotide additions and frequently were as complex as those of adults. The intestinal TCR-delta repertoire showed increasing restriction with age and, by 14 to 17 yr, the repertoire was oligoclonal and resembled the repertoire of individuals in the sixth to seventh decade. Moreover, the adult TCR-delta repertoire was almost identical at multiple sites throughout the intestine, suggesting a model in which gammadelta T cell clones, selected by ligands in the intestinal tract, undergo expansion and recirculation before lodging throughout the small intestine or colon.
43
Bartolomé-Casado, Raquel, Ole J. B. Landsverk, Sudhir Kumar Chauhan, Lisa Richter, Danh Phung, Victor Greiff, Louise F. Risnes, et al. "Resident memory CD8 T cells persist for years in human small intestine." Journal of Experimental Medicine 216, no. 10 (July 23, 2019): 2412–26. http://dx.doi.org/10.1084/jem.20190414.
Full textAbstract:
Resident memory CD8 T (Trm) cells have been shown to provide effective protective responses in the small intestine (SI) in mice. A better understanding of the generation and persistence of SI CD8 Trm cells in humans may have implications for intestinal immune-mediated diseases and vaccine development. Analyzing normal and transplanted human SI, we demonstrated that the majority of SI CD8 T cells were bona fide CD8 Trm cells that survived for >1 yr in the graft. Intraepithelial and lamina propria CD8 Trm cells showed a high clonal overlap and a repertoire dominated by expanded clones, conserved both spatially in the intestine and over time. Functionally, lamina propria CD8 Trm cells were potent cytokine producers, exhibiting a polyfunctional (IFN-γ+ IL-2+ TNF-α+) profile, and efficiently expressed cytotoxic mediators after stimulation. These results suggest that SI CD8 Trm cells could be relevant targets for future oral vaccines and therapeutic strategies for gut disorders.
44
Keshav, S., L. Lawson, L. P. Chung, M. Stein, V. H. Perry, and S. Gordon. "Tumor necrosis factor mRNA localized to Paneth cells of normal murine intestinal epithelium by in situ hybridization." Journal of Experimental Medicine 171, no. 1 (January 1, 1990): 327–32. http://dx.doi.org/10.1084/jem.171.1.327.
Full textAbstract:
Paneth cells in normal murine small intestine contain TNF mRNA that is readily detectable by in situ hybridization, unlike resident macrophages in lamina propria, which are negative. Northern blot analysis of whole tissue shows the presence of mRNA that has the same electrophoretic mobility as TNF mRNA from activated macrophages. A low level of TNF bioactivity, but no immunoreactivity, was detected in normal small intestine, and TNF production in resting Paneth cells appears to be post-transcriptionally controlled. Typical leukocyte surface membrane markers were not found on Paneth cells, but were expressed by the surrounding lamina propria macrophages. Paneth cells are thus epithelial cells with leukocyte-like secretory potential that may be important in intestinal physiology and pathology.
45
Panfilov, A. B., and I. V. Pestova. "Lymphoid tissue pattern in the walls of small and large intestines in American mink (Neovison vison)." Medical Immunology (Russia) 22, no. 1 (January 31, 2020): 153–56. http://dx.doi.org/10.15789/1563-0625-ltp-1811.
Full textAbstract:
When breeding minks, a lot of problems are associated with disturbances of reproduction, birth of weak offspring, metabolic disorders, weakening of immunity. Poor knowledge of the morphology of mink and lack of detailed information about their immune system is among appropriate reasons. The largest variety of antigens enter the body with food and water, through the wall of gastrointestinal tract. The first barrier to their penetration is lymphoid tissue associated with mucous membranes, thus causing changes in immune structures. Our purpose was to study the syntopia, morphology and quantitative characteristics of intestine-associated lymphoid tissue in American mink (Neovison vison). A biomaterial for the study was organocomplex of the small and large intestines from 11 American Minks at the age of 8 months, obtained from the fur farm “Vyatka” (Zonikha, Slobodsky district, Kirov region). In the walls of small and large intestines, both single and grouped lymphoid nodules are found. Single lymphoid nodules are detected in lamina propria of the mucous membrane and in the submucosa, along the entire length of the intestines, except of the ileum. Lymphoid nodules are round or oval, distributed diffusely, their density per 1 cm2 is in duodenum – 0.62±0.08; in jejunum – 1.88±0.32; in colon – 9.21±0.28; in rectum – 24.2±0.42. At the border of pyloric part between the stomach and duodenum, single lymphoid nodules form an intestinal-pyloric lymphoid ring; at the site of transition from rectum to the anal sphincter, the rectal lymphoid ring is observed. Abundance of lymphoid nodules in rectal area is associated with semi-voluntary management of animals, and retention of fecal mass in this part of intestine. By two lymphoid plaques are found in the duodenum; 6 to13, in the jejunum; one large striped (lingual) lymphoid plaque is found in the ileal wall; 1 to 3 plaques are found in the colonic wall. Presence of lymphoid plaques in colonic wall of American mink should be considered a protective/adaptive phenomenon, due to absence of coecum in the animals from Mustelid family. The revealed patterns of lymphoid tissue syntopia in American mink are associated with antigenicity of food substances and terms of their presence in the ileum, colon and rectum.
46
Dende, Chaitanya, Mihir Pendse, Daniel Propheter, Gabriella Quinn, and Lora V. Hooper. "Vitamin A regulates phagocytosis by resident macrophages of the small intestine." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 113.23. http://dx.doi.org/10.4049/jimmunol.208.supp.113.23.
Full textAbstract:
Abstract Intestinal Tim4+ CD4+ macrophages are a distinctive macrophage subset that express Tim4, a receptor for phosphatidylserine on dying apoptotic cells, Unlike other macrophage subsets, they do not depend on blood monocytes for their turnover, instead self-maintained in the small intestine. The signal(s) responsible for the self-maintenance and function of Tim4+ CD4+ macrophages is not known. We have discovered that maintenance of the gut resident Tim4+ CD4+ macrophage population depends on dietary vitamin A and its derivative retinoic acid (RA). Retinoic acid receptors, which direct RA-dependent transcription, were required for maintenance of Tim4+ CD4+ macrophages. Chemical blockade of retinoic acid receptor (RAR) signaling and macrophage-specific genetic inactivation of RARs in mice further revealed that macrophage-intrinsic RARα signaling was required for Timd4 expression and maintenance of Tim4+ CD4+ macrophages. Macrophage RARα signaling was furthermore essential for phagocytosis by Tim4+ CD4+ macrophages. Ongoing studies are examining the role of Tim4+ CD4+ macrophages and vitamin A in the clearance of apoptotic intestinal epithelial cells. Our findings reveal that vitamin A provides an essential dietary signal for the maintenance and function of a gut resident macrophage subset. Supported by Welch foundation grant I-1874
47
Shaw, Michael H., Nobuhiko Kamada, Yun-Gi Kim, and Gabriel Núñez. "Microbiota-induced IL-1β, but not IL-6, is critical for the development of steady-state TH17 cells in the intestine." Journal of Experimental Medicine 209, no. 2 (January 30, 2012): 251–58. http://dx.doi.org/10.1084/jem.20111703.
Full textAbstract:
TH17 cells are a lineage of CD4+ T cells that are critical for host defense and autoimmunity by expressing the cytokines IL-17A, IL-17F, and IL-22. A feature of TH17 cells at steady state is their ubiquitous presence in the lamina propria of the small intestine. The induction of these steady-state intestinal TH17 (sTH17) cells is dependent on the presence of the microbiota. However, the signaling pathway linking the microbiota to the development of intestinal sTH17 cells remains unclear. In this study, we show that IL-1β, but not IL-6, is induced by the presence of the microbiota in intestinal macrophages and is required for the induction of sTH17 cells. In the absence of IL-1β–IL-1R or MyD88 signaling, there is a selective reduction in the frequency of intestinal sTH17 cells and impaired production of IL-17 and IL-22. Myeloid differentiation factor 88–deficient (MyD88−/−) and germ-free (GF) mice, but not IL-1R−/− mice, exhibit impairment in IL-1β induction. Microbiota-induced IL-1β acts directly on IL-1R–expressing T cells to drive the generation of sTH17 cells. Furthermore, administration of IL-1β into GF mice induces the development of retinoic acid receptor–related orphan receptor γt–expressing sTH17 cells in the small intestine, but not in the spleen. Thus, commensal-induced IL-1β production is a critical step for sTH17 differentiation in the intestine, which may have therapeutic implications for TH17-mediated pathologies.
48
Hao, Ju, Yao Zhang, Li Tianyu, Shi Bo, Feng Shu, Shi Feng, Ji Chao, and Huang Ying. "Preliminary Investigation of the Diagnosis of Neonatal Congenital Small Bowel Atresia by Ultrasound." BioMed Research International 2019 (September 29, 2019): 1–6. http://dx.doi.org/10.1155/2019/7097159.
Full textAbstract:
Purpose. To assess the diagnostic value of ultrasonography (US) for congenital small bowel atresia (SBA) in neonates and their sonographic characteristics. Methods. A retrospective analysis was performed of 20 neonates who were confirmed with SBA by operation from March 2014 to January 2019. All the neonates have been scanned by US before surgery, and no one underwent barium enema or upper gastrointestinal imaging prior to US. Preoperation ultrasound characteristics about intestinal morphology and intestinal contents were collected, further to summarize the typical ultrasonic features of SBA. Results. Five cases were duodenal atresia, and 15 cases were jejuno-ileal atresia. Distended proximal intestines, liquid with tiny points in it, can be found in 20 neonates. The small intestine without any gas can be found in 20 neonates. Microcolon, no gas and other contents in it, can be found in 16 cases. Conclusions. The typical ultrasonic features of SBA include dilation in proximal intestines, small intestines, and microcolon. US is a promising modality in the clinical diagnosis of SBA.
49
Camerini, V., C. Panwala, and M. Kronenberg. "Regional specialization of the mucosal immune system. Intraepithelial lymphocytes of the large intestine have a different phenotype and function than those of the small intestine." Journal of Immunology 151, no. 4 (August 15, 1993): 1765–76. http://dx.doi.org/10.4049/jimmunol.151.4.1765.
Full textAbstract:
Abstract Intraepithelial lymphocytes (IEL) are found in both the small and the large intestine. We demonstrate that there are a number of striking phenotypic and functional differences between the two populations of IEL isolated from mice. In the large intestine, the majority of IEL express the alpha beta TCR, and among these TCR-alpha beta+ lymphocytes, CD4+ cells are as prevalent as CD8+ cells. In contrast, in the small intestine, most of the TCR-alpha beta+ IEL express CD8, and an increased percentage of cells express TCR-gamma delta. In addition, most TCR-gamma delta+ IEL isolated from the large intestine (LI-IEL) are CD4- CD8- cells, as compared to TCR-gamma delta+ IEL isolated from the small intestine (SI-IEL), which are predominantly CD8+. Furthermore, CD2 and the lymph node homing receptor, L-selectin, are expressed by most LI-IEL but not by SI-IEL. Furthermore, LI-IEL have much less cytolytic activity than SI-IEL. These data suggest that LI-IEL are a distinct population of lymphocytes that may have a different immunologic role than that of SI-IEL.
50
Zabel, Brian A., William W. Agace, James J. Campbell, Heidi M. Heath, David Parent, Arthur I. Roberts, Ellen C. Ebert, et al. "Human G Protein–Coupled Receptor Gpr-9-6/Cc Chemokine Receptor 9 Is Selectively Expressed on Intestinal Homing T Lymphocytes, Mucosal Lymphocytes, and Thymocytes and Is Required for Thymus-Expressed Chemokine–Mediated Chemotaxis." Journal of Experimental Medicine 190, no. 9 (November 1, 1999): 1241–56. http://dx.doi.org/10.1084/jem.190.9.1241.
Full textAbstract:
TECK (thymus-expressed chemokine), a recently described CC chemokine expressed in thymus and small intestine, was found to mediate chemotaxis of human G protein–coupled receptor GPR-9-6/L1.2 transfectants. This activity was blocked by anti–GPR-9-6 monoclonal antibody (mAb) 3C3. GPR-9-6 is expressed on a subset of memory α4β7high intestinal trafficking CD4 and CD8 lymphocytes. In addition, all intestinal lamina propria and intraepithelial lymphocytes express GPR-9-6. In contrast, GPR-9-6 is not displayed on cutaneous lymphocyte antigen–positive (CLA+) memory CD4 and CD8 lymphocytes, which traffic to skin inflammatory sites, or on other systemic α4β7−CLA− memory CD4/CD8 lymphocytes. The majority of thymocytes also express GPR-9-6, but natural killer cells, monocytes, eosinophils, basophils, and neutrophils are GPR-9-6 negative. Transcripts of GPR-9-6 and TECK are present in both small intestine and thymus. Importantly, the expression profile of GPR-9-6 correlates with migration to TECK of blood T lymphocytes and thymocytes. As migration of these cells is blocked by anti–GPR-9-6 mAb 3C3, we conclude that GPR-9-6 is the principal chemokine receptor for TECK. In agreement with the nomenclature rules for chemokine receptors, we propose the designation CCR-9 for GPR-9-6. The selective expression of TECK and GPR-9-6 in thymus and small intestine implies a dual role for GPR-9-6/CCR-9, both in T cell development and the mucosal immune response.