Academic literature on the topic 'Lymphocytes B intestinaux'
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Journal articles on the topic "Lymphocytes B intestinaux"
Artamonova, Z. A., and E. V. Namokonov. "NEW LABORATORY PARAMETERS IN THE DIAGNOSIS OF ACUTE MESENTERIC ISCHEMIA." Russian Clinical Laboratory Diagnostics 64, no. 8 (October 7, 2019): 490–92. http://dx.doi.org/10.18821/0869-2084-2019-64-8-490-492.
Full textWang, Caihong, Keely G. McDonald, Jacquelyn S. McDonough, and Rodney D. Newberry. "Murine isolated lymphoid follicles contain follicular B lymphocytes with a mucosal phenotype." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 4 (October 2006): G595—G604. http://dx.doi.org/10.1152/ajpgi.00525.2005.
Full textManzano, Manuel, Ana Clara Abadía‐Molina, Enrique‐García Olivares, Angel Gil, and Ricardo Rueda. "Dietary Nucleotides Accelerate Changes in Intestinal Lymphocyte Maturation in Weanling Mice." Journal of Pediatric Gastroenterology and Nutrition 37, no. 4 (October 2003): 453–61. http://dx.doi.org/10.1002/j.1536-4801.2003.tb12037.x.
Full textOsman, Mohammad, Janice Russell, and D. Neil Granger. "Lymphocyte-derived interferon-γ mediates ischemia-reperfusion-induced leukocyte and platelet adhesion in intestinal microcirculation." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 3 (March 2009): G659—G663. http://dx.doi.org/10.1152/ajpgi.90495.2008.
Full textGannon, Mark, Steve Brooks, Martin Kalmokoff, Jayadev Raju, Brent Selinger, Douglas Inglis, and Julia Green-Johnson. "Immunomodulatory effects of dietary fibre supplementation on lymphocyte populations, cytokine and immunoglobulin A production(39.16)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 39.16. http://dx.doi.org/10.4049/jimmunol.182.supp.39.16.
Full textAattouri, Najat, Mohammed Bouras, Daniel Tome, Ascension Marcos, and Daniel Lemonnier. "Oral ingestion of lactic-acid bacteria by rats increases lymphocyte proliferation and interferon-γ production." British Journal of Nutrition 87, no. 4 (April 2002): 367–73. http://dx.doi.org/10.1079/bjn2001527.
Full textShieh, Chi-Chang, Bhanu K. Sadasivan, Gary J. Russell, Michael P. Schön, Christina M. Parker, and Michael B. Brenner. "Lymphocyte Adhesion to Epithelia and Endothelia Mediated by the Lymphocyte Endothelial-Epithelial Cell Adhesion Molecule Glycoprotein." Journal of Immunology 163, no. 3 (August 1, 1999): 1592–601. http://dx.doi.org/10.4049/jimmunol.163.3.1592.
Full textMakori, Norbert, Alice F. Tarantal, Fabien X. Lü, Tracy Rourke, Marta L. Marthas, Michael B. McChesney, Andrew G. Hendrickx, and Christopher J. Miller. "Functional and Morphological Development of Lymphoid Tissues and Immune Regulatory and Effector Function in Rhesus Monkeys: Cytokine-Secreting Cells, Immunoglobulin-Secreting Cells, and CD5+ B-1 Cells Appear Early in Fetal Development." Clinical Diagnostic Laboratory Immunology 10, no. 1 (January 2003): 140–53. http://dx.doi.org/10.1128/cdli.10.1.140-153.2003.
Full textReynolds, J. D. "Evidence of extensive lymphocyte death in sheep Peyer's patches. I. A comparison of lymphocyte production and export." Journal of Immunology 136, no. 6 (March 15, 1986): 2005–10. http://dx.doi.org/10.4049/jimmunol.136.6.2005.
Full textJaimes, María C., Olga L. Rojas, Eric J. Kunkel, Nicole H. Lazarus, Dulce Soler, Eugene C. Butcher, Dorsey Bass, Juana Angel, Manuel A. Franco, and Harry B. Greenberg. "Maturation and Trafficking Markers on Rotavirus-Specific B Cells during Acute Infection and Convalescence in Children." Journal of Virology 78, no. 20 (October 15, 2004): 10967–76. http://dx.doi.org/10.1128/jvi.78.20.10967-10976.2004.
Full textDissertations / Theses on the topic "Lymphocytes B intestinaux"
Duran, Adrien. "Pathogénicité des lymphocytes dérivés de l'intestin dans la sclérose en plaques." Electronic Thesis or Diss., Bordeaux, 2022. http://www.theses.fr/2022BORD0097.
Full textMultiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system. The aetiology of MS is poorly understood but several factors, including genetic and environmental factors, are associated with susceptibility to MS. The gut, exposed to the intestinal microbiota, represents a major interface of immune cells with the environment. Studies in humans have shown that the composition of the gut microbiota is different between healthy subjects and MS patients. In the mouse model of MS, it has been observed that the composition of the gut microbiota influences the development of the disease. In addition, IgA-secreting B cells present in the cerebrospinal fluid of patients with active MS were found to mainly originated from the intestinal. In this context, we are interested in gut-derived B cells in the pathogenicity of MS. Historically, a role for B cells was proposed in MS following the discovery of antibodies in the cerebrospinal fluid of MS patients as it indicates an abnormal expansion of B cells. However, the recent success of B cell depletion therapies has highlighted a role for B cells independent of antibody production in MS pathology. We therefore aimed at determining the role of gut-derived B cells in MS pathology. To identify gut-derived B cells we used integrin b7 expression. Indeed, the expression of integrin b7 is initiated in naive lymphocytes at the inducer site of the intestine. Once expressed, the lymphocytes then enter the bloodstream and finally return to the intestine via the integrin b7 ligand, MADCAM, expressed by mucosal endothelial cells. The expression of integrin b7 by lymphocytes in the blood then allows us to identify the cells primed in the gut.We first studied the phenotype of these gut-derived B cells in healthy subjects in order to characterise them physiologically as they are poorly described in the literature. We were able to observe that IgD+ CD27+ B cells, also known as b7+ marginal B cells, have a more inflammatory profile compared to the memory B cells (IgD- CD27+) derived or not from the intestine and the marginal B cells not expressing the b7 integrin. Indeed, b7+ marginal B cells secrete higher levels of inflammatory cytokines, notably IL-6, TNFa and LT-a. Interestingly, this population also secretes higher levels of the immuno-regulatory cytokine IL-10.In a second step, we studied the characteristics of B cells in MS patients. We performed two sets of experiments. In the first set of experiments, we could observe that CD27+ B cells from some MS patients expressed more IL-6 than B cells from healthy donors as previously described. We determined that this higher secretion originates from b7+ memory B cells. In the second series of experiments, we did not observe any difference between patients and healthy donors for IL-6 expression, presumably because the patients studied were on immunomodulators/immunosuppressants and/or did not have active disease at the time of the sampling.In summary, in healthy subjects, B cells from the gut show both a more inflammatory and regulatory cytokine expression profile probably due to their exposure to the highly inflammatory environment of the intestine. In MS, we observed that the increased expression of IL-6 by B cells described in the literature is originated from b7+ B cells, suggesting that gut-derived B cells could be highly pathogenic in MS, notably by promoting inflammation in the central nervous system
Gaubert, Sophie. "La réponse IGA dans l'infection murine par Schistosoma mansoni : rôle des lymphocytes B1 dans l'immunité muqueuse anti-schistosome." Lille 1, 1998. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/1998/50376-1998-183.pdf.
Full textFoureau, David. "Mécanismes cellulaires et moléculaires TLR9-dépendants activés par T. gondii dans le système lymphoïde associé à la muqueuse intestinale." Thesis, Tours, 2008. http://www.theses.fr/2008TOUR4035/document.
Full textWe have investigated the role of TLR9 in the initiation of the immune response in the gut against Toxoplasma gondii. This innate immune receptor is widely expressed in the gut associated lymphoid tissue (GALT) : at the epithelial barrier and in the lamina propria. Expression of TLR9 is requiered in both these compartments to initiate a protective immune response against T. Gondii. Activation of TLR9 signaling pathways, by direct recognition of molecular motives expressed by T. gondii, induces the production of type I interferons (IFNs) in the small intestine. These interferons tregger the production of cryptdines (Crp-3 and -5) by paneth cells and their released into the lumen. Crps indirectly promote T cells (CD4 + IFN-y+) recruitmnent by enhancing the production of inflammatory chemokines. B-lymphocites express the TLR9 but do not contribute to the initiation of inflammatory response against T. gondii. However consecutively to the oral infection by the parasite, activated B cells amplify the inflammatory cytokine production (IFN-y), by effector T cells, via cell-cell interactions involving their mambrane bound TNF-a. In C57BL/6 mice, immune response against T. Gondii degenerates into a lethal ileitis. Regulatory T cells are naturally generated during infection. The sensibilisation of T regs by T. Gondii antigens, prior infection by the parasite, protects against the ileitis in our model. Sensibilized T regs overexpress gut homing receptors such as CCR5 AND a4ß7. By increasing their Th2 and Th3 cytokines production, sensibilized T regs readjust the cytokine balance in GALT of infected mice
Fesneau, Olivier. "Rôle du TGF-beta dans la biologie des lymphocytes Th17 déjà différenciés et leur impact dans l'inflammation chronique intestinale." Thesis, Lyon, 2019. https://n2t.net/ark:/47881/m6zw1k8c.
Full textThere is 10 to 100 more microorganism in the gut than human cells in the hole organism. Those microorganisms form the microbiota, and they are crucial to some vital functions like digestion. However, it is required to prevent from the microbiota dissemination in the organism. The immune system is highly involved in the control and the compartmentation of the microbiota. The immunosuppressive TGF-b prevents from over-activation of the immune cells versus the microbiota, and so protects from chronic inflammatory disease of the gut like Crohn’s disease or ulcerative colitis. TGF-b is also very involved in Th17 generation, a subset of cells with major role in microbiota control and maintenance of gut homeostasis. However, how TGFb acts on already differentiated Th17 is still under investigation. My results demonstrate that TGFb signaling in Th17 is required to maintain their lineage. In absence of TGF-b, Th17 switch to Th1 phenotype and produces important amount of inflammatory cytokines, leading to a strong inflammation of the gut, that may promotes cancer development
Reid, Timothy Dawson. "B lymphocyte activation and exhaustion in chronic HIV : novel surrogate markers of generalised immune activation and selective modulation of aberrant B cell responses using vasoactive intestinal peptide (VIP)." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/96898.
Full textENGLISH ABSTRACT: Introduction: Chronic HIV-1 infection is characterized by immune activation and dysregulation of immune homeostasis, which impacts on multiple immune cell types. The B-cell compartment, which plays an important role in the producing neutralizing antibodies, is also dysregulated in HIV- 1 infection. In this study we investigated peripheral blood B-cell subset distribution, and changes in expression of cellular activation, inhibition, and apoptosis signaling markers in both untreated chronic HIV-1 infected individuals and healthy uninfected controls. The neuropeptide immune modulator, vasoactive intestinal peptide (VIP) is known to selectively down-regulate activation of CD4+ T-cells in various disease settings including HIV-1, however to our knowledge, no studies have investigated the effect of VIP inhibition on B-cell activation. Materials & Methods: A total of 21 HIV+ve (CD4 count >250 cells/µl), and 19 HIV-ve individuals were recruited from the Emavundleni voluntary testing and counseling clinic in Crossroads, Western Province, South Africa. Whole blood was stained to distinguish B-cell subsets (activated memory (AM: CD21-CD27+), resting memory (RM: CD21+CD27+), mature naïve (MN: CD21+CD27-), or tissue-like memory (TLM: CD21loCD27lo). In addition expression of markers of B-cell activation (CD126, CD86, CD38, CD284, CD287), inhibition (CD72, CD85j, CD300a, CD305, CD307d), and apoptosis signaling (CD95), was assessed ex vivo by flow cytometry (BD FACSCanto II). For determination of functional responsiveness isolated B-cells (RosetteSep, Stemcell Technologies) were cultured for 18h (37°C, 5%CO2) without stimulation or stimulated with TLR ligands (LPS or R848). Stimulation experiments were also performed in the presence or absence of VIP. Results: Chronic HIV-1 infection affected B-cell subset distribution. The percentage (%) of TLM was increased by 59.24%, and %RM was decreased by 22.73% (both p<0.01). Total expression of the VIP receptor VPAC2 was decreased by 47.35% (p=0.0296). Subsets had a mixed phenotype ex vivo; HIV infection upregulated CD38 (by 59.56%, p=0.0004), CD72 (by 60.70%, p=0.0396), CD307d (by 68.63%, p=0.0015) on AM, while RM B-cells had increased expression of TLR4 (by 107.04%, p=0.0057) and TLR7 (by 208.14%, p=0.0199). TLM B cells (i.e. exhausted phenotype) displayed upregulated TLR7 (by 550%, p=0.0128) and CD307d (by 72.40% p=0.045) expression. MN B-cells had increased CD72 expression (by 70.98%, p=0.0026). R848 upregulated CD86 expression by 42.20% on AM (p<0.01), and by 56.06% on RM B-cells (p<0.01), which was significantly downregulated with VIP inhibition (both p<0.05). Similarly, CD95 expression on RM, TLM, and MN B-cells increased by 31.10% (p<0.001), 21.46% (p<0.01), and 39.92% (p<0.01) with R848 stimulation respectively, which was also significantly downregulated with VIP inhibition. Conclusion: These data indicate that B-cells in untreated HIV infection display increased levels of activation, and also the potential for increased susceptibility to apoptosis as evidenced by increased FAS (CD95) expression. VIP significantly down-regulated markers of activation, inhibition, and apoptosis signaling. Dysregulation of B-cells is thus apparent in asymptomatic stable chronic HIV-1 infection, which may impact on both inefficient neutralizing antibody production and hypergammaglobulinemia. The ability of VIP to prevent stimulationassociated marker upregulation may indicate that VIP is a potential therapeutic agent. Its immuno-modulatory properties were demonstrated to limit B-cell hyperactivation, and selectively down-regulate apoptosis and mark it out for further investigation.
AFRIKAANSE OPSOMMING: Inleiding: Immunaktivering en ongekoppelde immuun-homeostase is kenmerke van chroniese MIVinfeksie. Ons het perifere bloed B-sel subgroep-verspreiding, en veranderinge in die uitdrukking van merkers van aktivering, inhibisie, en apoptose in 'n onbehandelde MIV-1 besmettende groep ondersoek (in vergelyk met 'n gesonde onbesmettende kontrole). Die immuun-moduleerder, vasoaktiewe intestinale peptied (VIP) is bekend om aktivasie van geaktiveerde CD4+ T-selle te verminder, maar tot ons kennis, is daar geen studies wat die effek van VIP-inhibisie op B-sel aktivering ondersoek het, in die konteks van MIV-1 infeksie. Materiaal & Metodes: MIV+we individue (CD4-telling >250 selle/µl) , en MIVwe kontroles is gewerf uit die vrywillige toetsing en berading Emavundleni kliniek, Crossroads, Westelike Provinsie, Suid-Afrika. Bsel subgroepe is gedefinieer as geaktiveerde geheue (AM: CD21- CD27+ ), rusende geheue (RM: CD21+ CD27+ ), volwasse naïef (MN: CD21+ CD27- ), of weefsel-agtige geheue (TLM: CD21loCD27lo). Merkers van aktivering (CD126, CD86, CD38, CD284, CD287), inhibisie (CD72, CD85j, CD300a, CD305, CD307d), en apoptose signalering (CD95) is via vloeisitometrie (BD FACSCanto II) op B-selle ex vivo en ook op geïsoleerde B-selle (RosetteSep, Cell Technologies) ondersoek. Vir die bepaling van funksionele responsiwiteit, geïsoleerde B-selle (RosetteSep, StemCell Technologies) was vir 18h (37°C, 5%CO2) gekweek, sonder stimulasie of gestimuleer met TLR ligande (LPS of R848). Stimulasie eksperimente het ook in die teenwoordigheid of afwesigheid van VIP plaasgevind. Resultate: Chroniese MIV-1 infeksie het B-sel subset verspreiding geraak. Die persentasie (%) van TLM is verhoog deur 59,24%, en% RM het met 22.73% afgeneem (beide p <0,01). Totale uitdrukking van die VIP reseptor VPAC2 het met 47,35% afgeneem (p = 0,0296). Subgroepe het 'n gemengde ex vivo fenotipe; MIV-infeksie het CD38 (deur 59,56%, p=0,0004), CD72 (deur 60,70%, p=0,0396), CD307d (deur 68,63%, p=0,0015) op AM verhoog, terwyl RM Bselle het verhoogde uitdrukking van TLR4 (deur 107,04%, p=0,0057) en TLR7 (deur 208,14%, p=0,0199). TLM B-selle (die uitgeputtende fenotiep) het verhoogde TLR7 (deur 550%, p=0,0128) en CD307d (deur 72,40% p=0.045) uitdrukking gewys. MN B-selle het verhoogde uitdrukking van CD72 (deur 70,98%, p = 0,0026). R848 het CD86 uitdrukking op AM deur 42,20%, en op RM deur 56,06% toegeneem (beide p <0,01). Dit het met VIP inhibisie beduidend afgeneem (beide p <0.05). CD95 uitdrukking was soortgelyk verhoog op RM, TLM, en MN B-selle met 31.10% (p <0.001), 21,46% (p <0,01), en 39,92% (p <0,01) met R848 stimulasie. Al drie het beduidend afgeneem met VIP inhibisie. Gevolgtrekking: Hierdie data dui daarop dat B-selle in onbehandelde MIV-infeksie vertoon verhoogde aktiveringsvlakke, en ook die potensiaal vir verhoogde vatbaarheid vir apoptose soos bewys deur verhoogde uitdrukking van FAS (CD95). VIP het beduidend merkers van aktivering, inhibisie, en apoptose af-gereguleer. Wanfunksie van B-selle is dus in asimptomatiese stabiele chroniese MIV-1 infeksie duidelik, wat impak kan hê op beide oneffektiewe neutraliserende teenliggaampie produksie, en hiepergammaglobulinimie. Die vermoë van VIP stimulasie-verwante merker opregulasie te voorkom kan aandui dat VIP 'n potensiële terapeutiese agent is. VIP se immuno-moduleerende eiendomme is gedemonstreer om Bsel hieperaktiveering te beperk, en selektief apoptose afreguleer, en merk dit vir verdere ondersoek.
Uzzan, Mathieu. "Etude de la biologie des lymphocytes B et du mécanisme d'action du vedolizumab dans la rectocolite hémorragique et au cours de l'infection chronique à VIH." Thesis, Université de Paris (2019-....), 2019. http://www.theses.fr/2019UNIP7065.
Full textUlcerative Colitis (UC) is an inflammatory bowel disease (IBD) that leads to chronic inflammation of the rectum and the colon. Even though it is commonly accepted that it results from an exaggerated immune response toward the gut microbiota, the pathophysiology is still not fully understood. Among immune defects, many evidences exist supporting a disturbed B cell system, including the presence of (auto-)antibodies and the infiltration of the lamina propria by plasma cells. Using multiple advanced techniques including single-cell RNA sequencing and single-cell BCR sequencing we extensively characterized the B cell compartment in the blood and the intestinal mucosa of UC patients. We found that the colonic plasma cells phenotype was skewed toward an increased expression of IgG and IgA1 and an increased proportion of short-lived plasma cells. This increased turnover was reflected in the blood by the expansion of ?7+ plasmablasts, which correlated with disease activity and predicted disease course. Our second work focused on the mechanism of action of vedolizumab, a monoclonal antibody targeting the ?4?7 integrin, for both IBD and HIV. In a unique cohort of patients with concomitant IBD and HIV, we unexpectedly found that memory T cells within the lamina propria were not significantly affected. Conversely, lymphoid aggregates, mostly in the terminal ileum were massively impacted. These findings are being further explored and may change the paradigm regarding the mechanism of action of vedolizumab
Pesce, John Thomas. "Early events leading to the host protective Th2 immune response to an intestinal nematode parasite /." Download the dissertation in PDF, 2005. http://www.lrc.usuhs.mil/dissertations/pdf/Pesce2005.pdf.
Full textThiam, Fatou. "Effets de différents adjuvants de la famille de la toxine du choléra sur les lymphocytes T CD4 dans un modèle murin d'immunisation intrarectale avec des pseudoparticules virales de rotavirus." Phd thesis, Université de Bourgogne, 2011. http://tel.archives-ouvertes.fr/tel-00867205.
Full textBooks on the topic "Lymphocytes B intestinaux"
Geus, Bernard de. Differentiation and characterization of murine intestinal intraepithelial lymphocytes. s-Gravenhage: Pasmans Offsetdrukkerij BV, 1992.
Find full textBook chapters on the topic "Lymphocytes B intestinaux"
Naresh, Kikkeri N. "Gastrointestinal lymphomas." In Oxford Textbook of Medicine, edited by Jack Satsangi, 2892–902. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0301.
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