Mucosal T lymphocyte numbers are selectively reduced in integrin alpha E (CD103)-deficient mice
(1999) In Journal of Immunology 162(11). p.6641-6649- Abstract
- The mucosal lymphocyte integrin alpha E(CD103)beta 7 is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding alpha E, localized it to chromosome 11, and generated integrin alpha E-deficient mice. In alpha E-/- mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of alpha E beta 7 to E-cadherin expressed on epithelial cells. However, it was surprising that lamina propria T lymphocyte numbers were diminished, as E-cadherin is not expressed in the lamina propria. In contrast, peribronchial, intrapulmonary, Peyer's patch, and splenic T lymphocyte numbers were not reduced in alpha E-deficient mice. Thus, alpha E beta 7 was important... (More)
- The mucosal lymphocyte integrin alpha E(CD103)beta 7 is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding alpha E, localized it to chromosome 11, and generated integrin alpha E-deficient mice. In alpha E-/- mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of alpha E beta 7 to E-cadherin expressed on epithelial cells. However, it was surprising that lamina propria T lymphocyte numbers were diminished, as E-cadherin is not expressed in the lamina propria. In contrast, peribronchial, intrapulmonary, Peyer's patch, and splenic T lymphocyte numbers were not reduced in alpha E-deficient mice. Thus, alpha E beta 7 was important for generating or maintaining the gut and vaginal T lymphocytes located diffusely within the epithelium or lamina propria but not for generating the gut-associated organized lymphoid tissues. Finally, the impact of alpha E deficiency upon intestinal IEL numbers was greater at 3-4 wk of life than in younger animals, and affected the TCR alpha beta+ CD8+ T cells more than the gamma delta T cells or the TCR alpha beta+ CD4+CD8- population. These findings suggest that alpha E beta 7 is involved in the expansion/recruitment of TCR alpha beta+ CD8+ IEL following microbial colonization. Integrin alpha E-deficient mice will provide an important tool for studying the role of alpha E beta 7 and of alpha E beta 7-expressing mucosal T lymphocytes in vivo. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1114203
- author
- organization
- publishing date
- 1999
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Immunology
- volume
- 162
- issue
- 11
- pages
- 6641 - 6649
- publisher
- American Association of Immunologists
- external identifiers
-
- pmid:10352281
- ISSN
- 1550-6606
- language
- English
- LU publication?
- yes
- id
- c33adcca-97f4-4a08-bdba-9710976954e4 (old id 1114203)
- alternative location
- http://www.jimmunol.org/cgi/content/full/162/11/6641
- date added to LUP
- 2016-04-01 16:24:49
- date last changed
- 2018-11-21 20:41:13
@article{c33adcca-97f4-4a08-bdba-9710976954e4, abstract = {{The mucosal lymphocyte integrin alpha E(CD103)beta 7 is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding alpha E, localized it to chromosome 11, and generated integrin alpha E-deficient mice. In alpha E-/- mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of alpha E beta 7 to E-cadherin expressed on epithelial cells. However, it was surprising that lamina propria T lymphocyte numbers were diminished, as E-cadherin is not expressed in the lamina propria. In contrast, peribronchial, intrapulmonary, Peyer's patch, and splenic T lymphocyte numbers were not reduced in alpha E-deficient mice. Thus, alpha E beta 7 was important for generating or maintaining the gut and vaginal T lymphocytes located diffusely within the epithelium or lamina propria but not for generating the gut-associated organized lymphoid tissues. Finally, the impact of alpha E deficiency upon intestinal IEL numbers was greater at 3-4 wk of life than in younger animals, and affected the TCR alpha beta+ CD8+ T cells more than the gamma delta T cells or the TCR alpha beta+ CD4+CD8- population. These findings suggest that alpha E beta 7 is involved in the expansion/recruitment of TCR alpha beta+ CD8+ IEL following microbial colonization. Integrin alpha E-deficient mice will provide an important tool for studying the role of alpha E beta 7 and of alpha E beta 7-expressing mucosal T lymphocytes in vivo.}}, author = {{Schon, M P and Arya, A and Murphy, E A and Adams, C M and Strauch, U G and Agace, William and Marsal, J and Donohue, J P and Her, H and Beier, D R and Olson, S and Lefrancois, L and Brenner, M B and Grusby, M J and Parker, C M}}, issn = {{1550-6606}}, language = {{eng}}, number = {{11}}, pages = {{6641--6649}}, publisher = {{American Association of Immunologists}}, series = {{Journal of Immunology}}, title = {{Mucosal T lymphocyte numbers are selectively reduced in integrin alpha E (CD103)-deficient mice}}, url = {{http://www.jimmunol.org/cgi/content/full/162/11/6641}}, volume = {{162}}, year = {{1999}}, }