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Mucosal T lymphocyte numbers are selectively reduced in integrin alpha E (CD103)-deficient mice
M P Schön1, A Arya, E A Murphy
1Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|June 3, 1999
Summary
Integrin alpha E beta 7 is crucial for gut and vaginal T lymphocyte populations, particularly CD8+ intraepithelial lymphocytes, but not organized lymphoid tissues. This study generated alpha E-deficient mice to investigate its function in vivo.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Integrin alpha E (CD103) beta 7 is vital for mucosal lymphocyte homing and function.
- Its interaction with E-cadherin on epithelial cells is key for intraepithelial lymphocyte (IEL) localization.
Purpose of the Study:
- To investigate the role of integrin alpha E beta 7 in T lymphocyte development and localization.
- To characterize alpha E-deficient mice for studying mucosal immunity.
Main Methods:
- Cloning of the murine integrin alpha E gene.
- Generation and analysis of integrin alpha E-deficient (alpha E-/-) mice.
- Quantification of T lymphocyte populations in various tissues.
Main Results:
- Alpha E-/- mice exhibited reduced intestinal and vaginal IELs and lamina propria T cells.
- T lymphocyte numbers in organized lymphoid tissues (Peyer's patches, spleen) were unaffected.
- The deficiency impacted TCR alpha beta+ CD8+ IELs more significantly, especially post-microbial colonization.
Conclusions:
- Integrin alpha E beta 7 is essential for generating/maintaining diffuse gut and vaginal T lymphocytes, not organized lymphoid tissues.
- Alpha E beta 7 plays a role in the expansion and recruitment of specific IEL subsets, particularly TCR alpha beta+ CD8+ T cells.
- Alpha E-deficient mice are valuable tools for in vivo studies of mucosal T cell immunity.