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Academic literature on the topic 'Integrin b7'

Author: Grafiati
Published: 18 May 2024

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Journal articles on the topic "Integrin b7"

1

Sato, Yuichiro, Kiminori Matsubara, Takanori Kubo, Hirobumi Sunayama, Yuta Hatori, Kinjiro Morimoto, and Toshio Seyama. "High Mannose Binding Lectin (PFL) from Pseudomonas fluorescens Down-Regulates Cancer-Associated Integrins and Immune Checkpoint Ligand B7-H4." Cancers 11, no. 5 (April 30, 2019): 604. http://dx.doi.org/10.3390/cancers11050604.

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Pseudomonas fluorescens lectin (PFL), which belongs to the high mannose (HM)-binding OAAH (Oscillatoria agardhii agglutinin homologue) lectin family, induces cancer cell death. However, the detailed mechanisms underlying this process have not yet been elucidated. We found that PFL decreased various integrins as well as EGFR in cancer cells by promoting internalization and autophagic degradation of these molecules, subsequently inducing caspase-8 dependent cell apoptosis. As revealed by an ex vivo angiogenesis assay using the rat aortic model, PFL inhibited neovascularization in a dose-dependent manner, which was potentially mediated by down-regulation of endothelium integrins. Interestingly, PFL also down-regulated B7-H4 in cancer cells, which has been implicated as a negative regulator of T cell-mediated immunity. We found that B7-H4 co-localized with β3 integrin in MKN28 gastric cancer cells. siRNA silencing of B7-H4 in MKN28 cells decreased expression of β3 integrin, suggesting physical and functional association between these molecules. Direct interaction of PFL with integrin αvβ3 or B7-H4 was examined by surface plasmon resonance analysis, which detected high affinity glycan-dependent binding to PFL. These investigations suggest that PFL interaction with cell surface integrins is a key process for the anti-cancer activities of PFL.
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Damle, N. K., K. Klussman, G. Leytze, A. Aruffo, P. S. Linsley, and J. A. Ledbetter. "Costimulation with integrin ligands intercellular adhesion molecule-1 or vascular cell adhesion molecule-1 augments activation-induced death of antigen-specific CD4+ T lymphocytes." Journal of Immunology 151, no. 5 (September 1, 1993): 2368–79. http://dx.doi.org/10.4049/jimmunol.151.5.2368.

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Abstract Integrin ligands intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) can efficiently costimulate proliferation of resting T cells but not that of Ag-specific T cells. In contrast, CD28 ligand B7 and CD2 ligand leukocyte function-associated Ag (LFA-3) can support IL-2 synthesis and proliferation of Ag-specific T cells more efficiently than that of resting T cells. The molecular basis for this differential costimulation of T cells is poorly understood. In this study, using mAb and soluble IgC gamma 1 chimeras of these adhesion molecules, we demonstrate that coligation of the TCR and CD11a/CD18 (LFA-1/beta 2 integrin) or CD29/CD49d (very late activation Ag-4/beta 1 integrin) using anti-TCR mAb and either ICAM-1 or VCAM-1 induces activation-dependent death of DRw6-specific CD4+ T cells. Similar coligation of the TCR with CD2 or CD28 using either mAb or ligands LFA-3 or B7 not only lacked the ability to induce death but also failed to reverse or inhibit integrin-facilitated death of DRw6-specific T cells. Each of these ligands augmented anti-TCR mAb-induced transcription of IL-2 and IL-4 genes. Exogenous addition of IL-2 and IL-4 did not reverse the integrin-supported T cell death. The death-promoting costimulatory effects of ICAM-1 and VCAM-1 were observed with Ag-specific chronically stimulated T cells but not with either resting T cells or those activated in short-term cultures. Treatment of T cells with cyclosporin A or a protein tyrosine kinase inhibitor herbimycin A inhibited ICAM-1 or VCAM-1-promoted activation-induced T cell death. The Ag-specific T cells that survived death-promoting effects of ICAM-1 or VCAM-1 proliferated efficiently upon restimulation with these ligands. Exposure of DRw6-specific T cells to DRw6+ B7+ ICAM-1+ LFA-3+ VCAM-1+ APC but not DR3+ B7+ ICAM-1+ LFA-3+ VCAM-1+ APC induced death of these T cells. This effect was blocked by pretreatment of T cells with mAb directed at CD18 or CD29 but not with those against CD2 or CD28. Taken together, these results suggest that TCR-directed engagement of integrins by their ligands ICAM-1 or VCAM-1 induces activation-dependent death of some perhaps more differentiated Ag-specific T cells and this may be an important homeostatic mechanism by which functional expression of Ag-specific T cells is regulated during an ongoing immune response.
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Graham, Zachary, Chad Touchberry, Paige Geiger, Anisha Gupte, Gregory Bomhoff, and Philip Gallagher. "Integrin Signaling in Heat-shocked Rat Skeletal Muscle Following Eccentric Exercise." Medicine & Science in Sports & Exercise 42 (October 2010): 58. http://dx.doi.org/10.1249/01.mss.0000389357.14247.b7.

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4

Damle, N. K., K. Klussman, G. Leytze, S. Myrdal, A. Aruffo, J. A. Ledbetter, and P. S. Linsley. "Costimulation of T lymphocytes with integrin ligands intercellular adhesion molecule-1 or vascular cell adhesion molecule-1 induces functional expression of CTLA-4, a second receptor for B7." Journal of Immunology 152, no. 6 (March 15, 1994): 2686–97. http://dx.doi.org/10.4049/jimmunol.152.6.2686.

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Abstract Costimulation by the CD28 ligand B7/BB1 plays an important role during T cell proliferation primarily by augmenting synthesis of IL-2 and other cytokines. Resting CD4+ T cells express CD28 but not CTLA-4 on their surface. Costimulation of T cells with ICAM-1 or VCAM-1 induced CTLA-4 expression and up-regulated CD28 expression. CD28 and CTLA-4 were independently distributed on the surface of activated T lymphoblasts. When co-immobilized with anti-TCR mAb both anti-CD28 and anti-CTLA-4 mAb augmented T cell proliferation. Although anti-CD28-mediated augmentation of T cell proliferation was stronger than that seen with anti-CTLA-4 mAb, together these two mAb caused supraadditive augmentation of T cell proliferation. The augmentation of the effects of anti-CD28 mAb by anti-CTLA-4 mAb was greater at low occupancy of CD28 by anti-CD28 mAb. Costimulation of CD28+ CTLA-4+ T cells with anti-CTLA-4 caused three- to fivefold increase in IL-2 production, whereas similar treatment with anti-CD28 caused > 40-fold increase. The costimulatory effect of B7 on primed T cells was partially inhibited by Fab anti-CD28 mAb. Anti-CTLA-4 mAb alone did not inhibit B7-induced response but caused modest increase in the inhibitory effect of anti-CD28 Fab. On integrin-mediated costimulation, Ag-specific CD4+ T cell lines also up-regulated their CTLA-4 expression, and proliferation of these cells was augmented by anti-CTLA-4 mAb. Unlike that of CD28, ligation of CTLA-4 alone failed to mobilize intracellular [Ca2+]. However, coligation of CTLA-4 and TCR induced stronger [Ca2+] response in Ag-specific T cell lines than that seen with TCR alone. These results suggest that integrin-costimulated T cells express CTLA-4 and can be costimulated via CTLA-4. Optimal development of various immune functions may involve combined costimulation via both CD28 and CTLA-4.
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Hacsek, G., T. Örmälä, J. M. Kantele, and E. Savilahti. "B7 Integrin Expression of Lamina Propria Lymphocytes Increases in Rectum and Colon During Infancy 66." Pediatric Research 42, no. 3 (September 1997): 396. http://dx.doi.org/10.1203/00006450-199709000-00086.

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Rodger, B., I. Hoti, H. Gordon, J. Lindsay, and A. Stagg. "P007 Identification and characterisation of intestine-derived circulating resident memory T cells (ex-Trm) in health and Inflammatory Bowel Disease." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S128. http://dx.doi.org/10.1093/ecco-jcc/jjab076.136.

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Abstract Background Tissue resident memory T cells (Trm) persist in peripheral tissues where they protect against pathogens but can also contribute to inflammatory disease. Recent work shows that Trm can re-enter the circulation and give rise to new effector T cell and Trm populations in secondary tissue sites. Such ‘ex -Trm’ derived from the skin co-express the residency marker CD103 with cutaneous leukocyte antigen (CLA), a marker associated with skin tropism. Many T cells in the human intestine are Trm but it is unknown whether these cells re-enter the circulation; the existence of gut-derived ex-Trm would have important implications for IBD treatment targeting the recruitment of circulating gut-homing cells. Here, we identify a population of blood cells that co-express CD103 and the gut-homing integrin a4b7 and determine how they are changed in IBD. Methods Peripheral blood mononuclear cells (PBMCs) were isolated from healthy volunteers and patients with active IBD (Crohn’s disease or ulcerative colitis). Cell surface staining and multi-colour flow cytometry were used to identify CD4+ and CD8+ subsets of antigen experienced (CD45RA-) conventional T cells (abTCR+) and determine expression of markers associated with tissue tropism and residency. Results Staining with antibodies to CD103 and b7 integrin were used to define CD103b7+a4b7+ putative gut ex-Trm based on the excess per cell expression of b7 resulting from its contribution to both integrins. A separate CD103b7+a4b7- population defined by 1:1 expression of CD103 and b7 contained CLA+ skin ex-Trm. Gut ex-Trm comprised 0.3% total circulating CD8+ T cells (range 0.02–1.4%), and 1.2% CD4+ T cells (range 0.3–3%). Gut and skin ex-Trm were phenotypically similar; both expressed the residency associated markers CD101 and CD9 but lacked expression of CD69. Gut ex-Trm were phenotypically distinct from both traditional CD103-a4b7+ gut tropic CD45RA- antigen-experienced T cells and naïve T cells; significantly more gut ex-Trm expressed CD101 and CD9 and fewer expressed CD27. The proportion of gut ex-Trm did not differ between heath and IBD. However, the ratio of gut:skin ex Trm was significantly reduced in active Crohn’s disease but not ulcerative colitis indicating a selective reduction in the population derived from the intestine. Conclusion A putative population of gut-derived ex-Trm can be identified in the blood of healthy controls and IBD patients. This population has a distinctive phenotype similar to that of previously described skin-derived ex-Trm. Circulating ex-Trm could link discreet areas of intestinal inflammation in Crohn’s disease and there is a selective loss of the gut ex-Trm population from the blood of these patients. The role of ex-Trm in IBD merits further study.
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Tsai, FC. "143B: CORRELATION BETWEEN THE EXPRESSION PATTERN OF INTEGRIN ALPHA V AND CANCER INVASION IN CANCERS." Plastic and Reconstructive Surgery 125, Supplement (June 2010): 96. http://dx.doi.org/10.1097/01.prs.0000371877.11202.b7.

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Sumen, Cenk, Michael L. Dustin, and Mark M. Davis. "T cell receptor antagonism interferes with MHC clustering and integrin patterning during immunological synapse formation." Journal of Cell Biology 166, no. 4 (August 16, 2004): 579–90. http://dx.doi.org/10.1083/jcb.200404059.

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T cell activation by nonself peptide–major histocompatibility complex (MHC) antigenic complexes can be blocked by particular sequence variants in a process termed T cell receptor antagonism. The inhibition mechanism is not understood, although such variants are encountered in viral infections and may aid immune evasion. Here, we study the effect of antagonist peptides on immunological synapse formation by T cells. This cellular communication process features early integrin engagement and T cell motility arrest, referred to as the “stop signal.” We find that synapses formed on membranes presenting antagonist–agonist complexes display reduced MHC density, which leads to reduced T cell proliferation that is not overcome by the costimulatory ligands CD48 and B7-1. Most T cells fail to arrest and crawl slowly with a dense ICAM-1 crescent at the leading edge. Similar aberrant patterns of LFA-1/ICAM-1 engagement in live T–B couples correlate with reduced calcium flux and IL-2 secretion. Hence, antagonist peptides selectively disable MHC clustering and the stop signal, whereas LFA-1 valency up-regulation occurs normally.
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Maile, Laura A., and David R. Clemmons. "Integrin-Associated Protein Binding Domain of Thrombospondin-1 Enhances Insulin-Like Growth Factor-I Receptor Signaling in Vascular Smooth Muscle Cells." Circulation Research 93, no. 10 (November 14, 2003): 925–31. http://dx.doi.org/10.1161/01.res.0000101754.33652.b7.

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Hermangild Kottoor, S., H. Ibraheim, P. Polychronis, B. Senthuran, E. Jameson, M. Samaan, P. Irving, and N. Powell. "P009 Integrin-b7+ cytotoxic MAIT cells are expanded in the colon of Ulcerative Colitis patients, correlate with disease severity and are targeted by vedolizumab therapy." Journal of Crohn's and Colitis 16, Supplement_1 (January 1, 2022): i140. http://dx.doi.org/10.1093/ecco-jcc/jjab232.138.

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Abstract Background Mucosal-associated invariant T (MAIT) cells are major histocompatibility complex (MHC) class Ib-restricted innate-like lymphocytes with anti-bacterial functions that are enriched at mucosal sites. Their role in ulcerative colitis (UC) is unknown. Methods Colonic biopsies and peripheral blood were collected from patients with active UC (n=34) and healthy control subjects (n=14). Peripheral blood mononuclear cells (PBMC) and Lamina propria mononuclear cells (LPMC) were isolated and activated in vitro with PMA/ionomycin followed by surface and intracellular staining and multiparametric flow cytometry analysis. T cell populations, including gamma delta T cells (TCR gamma delta+), iNKT cells (TCR Vα24-Jα18+), MAIT cells (TCR Vα7.2+ CD161+), CD4, CD8 T cells and their intracellular expression of IL17A, TNF, IFN-g, IL22, IL13 and granzyme B (GZMB) were determined. MAIT cells were further characterised as CD8+, CD4+, CD8 CD4 double positive (DP), CD8 CD4 double negative (DN) cells and expression of the gut homing integrin-b7. Results DN cells were the most common MAIT subset in the colon and were significantly increased in both UC patients and HC subjects compared to peripheral blood. In UC, DN MAIT cells exhibited a cytotoxic phenotype, with significantly higher production of Granzyme B (median 45.0% of cells) compared to DN MAIT cells in HC (median 17%, P<0.005). DN MAIT cells in UC gut also co-produced significantly higher proportion of IL17A (median 22% in UC vs 7% in HC, P<0.006) and TNF (median 61% in UC vs 10% in HC, P<0.02) compared to DN MAIT cells from HC. In UC patients, the proportional abundance of cytotoxic DN MAIT cells accumulating in the colon significantly correlated with disease activity (UCEIS) score (r2=0.34, P<0.0007). The number of DN MAIT cells expressing integrin-b7 was also significantly higher in UC patients compared to HC (median 66% in UC vs 32% in HC, p<0.001). In UC patients initiated on vedolizumab therapy, the proportional abundance of cytotoxic, DN MAIT cells accumulating in the colon significantly fell at week 14 in comparison with their pre-treatment abundance (median 25% vs 51%, P<0.001). Following vedolizumab induction, the reduction in the abundance of colonic cytotoxic DN MAIT cells correlated with endoscopic improvement (r2=0.45, p=0.0085). Conclusion DN MAIT cells with cytolytic activity and augmented expression of multiple cytokines are enriched in the colon of UC patients in numbers that correlate with the magnitude of mucosal injury. Vedolizumab treatment reduces DN MAIT cell accumulation in the colon and the magnitude of reduction correlates with treatment response.
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Book chapters on the topic "Integrin b7"

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Lutz, M. B., C. Winzler, C. Aβmann, and P. Ricciardi-Castagnoli. "Priming of T Cells with Dendritic, Macrophage and B Cell Lines in Vivo Requires More than Surface Expression of MHC II and B7 Molecules - Possible Role of CD44 and Integrins." In Advances in Experimental Medicine and Biology, 413–17. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_93.

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P. Chapoval, Svetlana, and Andrei I. Chapoval. "Costimulation in Allergic Asthma: The Roles of B7 and Semaphorin Molecules." In Recent Advances in Asthma Research and Treatments. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102631.

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It is well established that allergic asthma is T cell-driven disease where CD4+ T cells of Th2 phenotype play a critical role in disease initiation and maintenance. There are several critical steps in the induction of Th2 type immune response to the allergen. The first critical step is the antigen processing and presentation of allergen-derived peptides in the context of specific major histocompatibility Class II (MHCII) molecules by antigen-presenting cells (APC). Recognition of this complex by T cell receptor (TCR) and interaction of costimulatory ligands with corresponding receptors represents the second step in T cell activation. As the third part of optimal T cell differentiation, proliferation, and expansion, several cytokines, integrins, and chemokines get involved in the fine-tuning of DC-T cell interaction and activation. Multiple recent evidences point to the selected members of B7 and semaphorin families as important checkpoints providing a fine-tuning regulation of immune response. In this book chapter, we discuss the properties of costimulatory molecules and address their roles in allergic asthma.
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Conference papers on the topic "Integrin b7"

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Kirkemo, Finn. "Fasteners: Strength and Quality Requirements." In ASME 2014 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/pvp2014-28719.

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Heavy hex nuts may be selected with similar hardness to the studs to avoid stripping of nut threads for pressure containing (closure bolting) and primary load bearing bolting. However, industry specification for subsea production systems, e.g. such as API Specifications 6A, 16A, 16C, and 17D, allows the use of low strength heavy hex nuts, e.g. ASTM A194 Grade 2HM or 7M, to be applied together with high strength studs, e.g. ASTM A320 Grades L43 or L7. In the refining and chemical industries the common practice is to use ASTM A193 B7 studs with 2H nuts. Calculations and testing of nuts have been performed and capacity formulas have been established for nut structural capacities. Guidance is given on selecting nut strength/hardness to avoid stripping of nut threads. ASTM specifications give minimum quality requirements during manufacture. A brief review of standard quality requirements is given and guidance for additional requirements for high integrity fasteners in order to have equivalent quality as pressure containing forgings is given. The results from this paper may be used as background for requirements in code updates and purchaser specifications.
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Brewer, Jonathan, and Colton Sheets. "Analytical and Experimental Assessment of Short Bolted Flange Nuts Subjected to Tensile Loads for Development of Mitigation Strategy." In 2022 14th International Pipeline Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/ipc2022-87744.

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Abstract Analytical and experimental methods were used to develop a strategy for assessing short bolted threaded connections (studs and nuts) under tensile loading. Short bolting occurs when a threaded connection has some number of threads that remain unengaged. This unthreaded length is called shortfall. Analytical efforts primarily focused on predicting the failure loads and failure modes associated with various levels of shortfall. An analytical methodology for assessing short bolting is important as it allows an end user to develop a threat prioritization or integrity management program based on a desired level of risk tolerance. A risk averse, conservative approach could require that all nuts have sufficient engagement length to produce a tensile overload failure of the stud. A risk tolerant approach might utilize predicted failure load as an integrity criterion instead of predicted failure mode. Development of the analytical models, including a review of existing literature, is described within this paper. The primary output of the analytical models includes the expected failure load as a function of the threaded connection engagement length and the critical “transition engagement length” at which the failure mode changes from thread shear to stud tension. Above this engagement length, the threaded connection is expected to fail due to tensile overload of the stud and is “full strength”. Below this engagement length, the threaded connection is expected to fail by thread shearing, at a load lower than the tensile strength of the stud. To validate the analytical approaches, a series of full-scale tests were conducted using 1.5-inch and 2-inch diameter B7 studs (ASTM A193) and ASTM A194 2-H heavy hex nuts. Laboratory evaluation of the threaded connections consisted of dimensional measurements and tension-to-failure testing. Tension-to-failure testing consisted of applying increasing tension loads to the threaded connections with varying shortfall lengths. The failure mode of the test was recorded and compared to predictions from the analytical models. A total of 18 tension-to-failure tests were performed. If nut and stud material and geometric properties are known, it was determined that analytical calculations based on SAE 770420 with a modified shear stress capacity defined as 0.5*UTS (ultimate tensile strength) results in the best match to the test results. The transition engagement length matched within 2% for both stud sizes. However, if the nut and stud material and geometric properties are unknown, analytical calculations based on ASME B1.1, Appendix B, with shear stress capacity defined as 0.5*UTS were found to be more appropriate. The transition engagement length matched within 2% for both stud sizes. Based on these analysis and testing results, a multilevel inspection program was defined to assess an asset system.
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