Topic
Integrin Alpha-E
About: Integrin Alpha-E is a research topic. Over the lifetime, 13 publications have been published within this topic receiving 1471 citations.
Papers
TL;DR: The results indicate that αEβ7 does not act as a homing receptor, and that the expression of the site‐specific marker αE does not correlate with a distinct homing behavior.
Abstract: The integrin alpha E (HML-1, alpha IEL, alpha M290) is largely expressed on lymphocytes in epithelial sites, especially the gut mucosa. We investigated whether alpha E has any role in homing or delineates a phenotype with distinct migratory behavior. Lymph node T cells were stimulated for 5 days with anti-CD3 in the presence or absence of transforming growth factor (TGF)-beta 1 to generate alpha E+ or alpha E- cells, respectively. The two populations were then tested for their homing properties in mice. Both alpha E+ (TGF-beta-treated) and alpha E- (control) cells of either CD4+ or CD8+ subset had a low capacity to enter the gut and showed the same homing behavior with respect to a variety of other organs. The same was true for alpha E+ and alpha E- cells that had been briefly stimulated with anti-CD3 (24 h) and then allowed to return to a resting state before injection, though in this case both populations showed a greater capacity to recirculate through lymphoid tissue than was seen with fully activated cells. The results indicate that alpha E beta 7 does not act as a homing receptor, and that the expression of the site-specific marker alpha E does not correlate with a distinct homing behavior.
94 citations
TL;DR: A role for αEβ7 in interactions with the intestinal endothelium that may have implications for intestinal T cell homing or functional responses is suggested, and there was evidence for an αE β7 ligand on intestinal endothelial cells in vivo, as αEαβ7 expression enhanced lymphocyte binding around vessels in the lamina propria in tissue sections.
Abstract: Integrins are important for T cell interactions with endothelial cells Because the integrin alpha(E)beta(7) is expressed on some circulating gut-homing T cells and as T cell numbers are reduced in the intestinal lamina propria of alpha(E)-deficient mice, we evaluated whether alpha(E)beta(7) mediates binding to intestinal endothelial cells We found that anti-alpha(E)beta(7) mAbs partially blocked the binding of cultured intraepithelial T cells to human intestinal microvascular endothelial cells (HIMEC) Furthermore, alpha(E)beta(7)-transfected K562 cells bound more efficiently than vector-transfected K562 cells to HIMEC Finally, HIMEC bound directly to an alpha(E)beta(7)-Fc fusion protein These interactions were partially blocked by anti-alpha(E)beta(7) mAbs, and endothelial cell binding to the alpha(E)beta(7)-Fc was dependent upon the metal ion-dependent adhesion site within the alpha(E) A domain Of note, the HIMEC lacked expression of E-cadherin, the only known alpha(E)beta(7) counterreceptor as assessed by functional studies, flow cytometry, and RT-PCR Thus, HIMEC/alpha(E)beta(7) binding was independent of E-cadherin In addition, this interaction appeared to be tissue selective, as HIMEC bound to the alpha(E)beta(7)-Fc, whereas microvascular endothelial cells from the skin did not Finally, there was evidence for an alpha(E)beta(7) ligand on intestinal endothelial cells in vivo, as alpha(E)beta(7) expression enhanced lymphocyte binding around vessels in the lamina propria in tissue sections Thus, we have defined a novel interaction for alpha(E)beta(7) at a nonepithelial location These studies suggest a role for alpha(E)beta(7) in interactions with the intestinal endothelium that may have implications for intestinal T cell homing or functional responses
71 citations
Journal Article•
TL;DR: It is demonstrated that synovial T lymphocytes have the capacity to express the 'mucosal-type' integrin alpha E beta 7, possibly due to high levels of intra-articular TGF-beta 1.
Abstract: The synovial expression of the mucosal lymphocyte integrin alpha E beta 7 and its ligand E-cadherin was analysed in order to study the relationship between T lymphocytes of the gastrointestinal tract and the synovium in patients with rheumatoid arthritis (RA). Immunohistochemical evaluation of synovium revealed that the alpha E beta 7-expression was detectable in 16 of the 38 samples examined. A concomitant examination on circulating lymphocytes by flow cytometry showed that alpha E beta 7-expressing lymphocytes occur less frequently in peripheral blood (PB). In vitro culture of lymphocytes increased the alpha E beta 7-expression on synovial lymphocytes six-fold, whereas PB lymphocytes expressed a two-fold increase. The addition of PHA to the culture medium did not dramatically increase the alpha E beta 7-expression on synovial lymphocytes, in contrast to PB lymphocytes where a 24-fold increase was detected. The addition of TGF-beta 1 to the culture of PB lymphocytes increased the alpha E beta 7-expression three-fold. E-cadherin expression was found in all synovial tissues analysed by immunohistochemistry. These results demonstrate that synovial T lymphocytes have the capacity to express the 'mucosal-type' integrin alpha E beta 7, possibly due to high levels of intra-articular TGF-beta 1. This expression might be of physiological importance since E-cadherin, the ligand for alpha E beta 7, is richly expressed by synoviocytes. In addition, the results indicate that a high in vivo expression of alpha E beta 7 is suppressed in the synovial tissue by a hitherto unknown mechanism.
48 citations
TL;DR: More than 80% of the gamma delta T-cells in BAL fluid expressed alpha E beta 7 at all time-points, suggesting a role for these cells in the pathogenesis of bleomycin-induced lung fibrosis.
Abstract: CD4, CD8, and gamma delta T-cells located in the epithelium express the integrin alpha E beta 7 that binds to E-cadherin on the epithelium. Gamma delta T-cells mediate specific cellular immune functions and can recognize damaged cells directly. It was, therefore, of interest to analyse the presence of gamma delta T-cells and the expression of alpha E beta 7 on gamma delta T-cells in the bleomycin (BLM) model of pulmonary fibrosis. Lung fibrosis was induced by a single intratracheal instillation of BLM (0.125 U.mouse-1), and bronchoalveolar lavage (BAL) T-cell subpopulations were examined at various time-points for the expression of the integrin alpha E beta 7 by flow cytometry. CD4+ T-cells accounted for about 40% of the lymphocytes, compared to about 10% of CD8+ T-cells and 10-14% gamma delta T-cells. Within the CD4+ T-cell population the proportion of alpha E beta 7+ cells decreased between Days 2 and 22 from 36 to 11%. The percentage of alpha E beta 7+ CD8+ T-cells increased at the same time from 4 to 68%. However, more than 80% of the gamma delta T-cells in BAL fluid expressed alpha E beta 7 at all time-points. The surface-expression of this integrin on gamma delta T-cells was 2-3 times higher than on CD4+ or CD8+ T-cells. This predominant expression of alpha E beta 7 on gamma delta T-cells suggests a role for these cells in the pathogenesis of bleomycin-induced lung fibrosis.
20 citations
17 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
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| 2021 | 1 |
| 2018 | 1 |
| 2006 | 1 |
| 2001 | 1 |
| 2000 | 1 |
| 1999 | 1 |