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Mucosal T Lymphocyte Numbers Are Selectively Reduced in Integrin αE (CD103)-Deficient Mice

Authors :
Michael P. Schön
Anu Arya
Elizabeth A. Murphy
Cassandra M. Adams
Ulrike G. Strauch
William W. Agace
Jan Marsal
John P. Donohue
Helen Her
David R. Beier
Sara Olson
Leo Lefrancois
Michael B. Brenner
Michael J. Grusby
Christina M. Parker
Source :
The Journal of Immunology. 162:6641-6649
Publication Year :
1999
Publisher :
The American Association of Immunologists, 1999.

Abstract

The mucosal lymphocyte integrin αE(CD103)β7 is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding αE, localized it to chromosome 11, and generated integrin αE-deficient mice. In αE−/− mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of αEβ7 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 αE-deficient mice. Thus, αEβ7 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 αE deficiency upon intestinal IEL numbers was greater at 3–4 wk of life than in younger animals, and affected the TCR αβ+ CD8+ T cells more than the γδ T cells or the TCR αβ+ CD4+CD8− population. These findings suggest that αEβ7 is involved in the expansion/recruitment of TCR αβ+ CD8+ IEL following microbial colonization. Integrin αE-deficient mice will provide an important tool for studying the role of αEβ7 and of αEβ7-expressing mucosal T lymphocytes in vivo.

Subjects

Subjects :
Immunology
Immunology and Allergy

Details

ISSN :
15506606 and 00221767
Volume :
162
Database :
OpenAIRE
Journal :
The Journal of Immunology
Accession number :
edsair.doi...........99c7e8ce3776b8c7b1f2641eb9a01011
Full Text :
https://doi.org/10.4049/jimmunol.162.11.6641