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Published on: April 21, 2015
Cutaneous inflammatory disorder in integrin alphaE (CD103)-deficient mice
M P Schön1, M Schön, H B Warren
1Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|November 22, 2000
Summary
Integrin alpha(E)beta(7) deficiency surprisingly led to inflammatory skin lesions in mice, suggesting a role in immune regulation and a risk factor for skin disease when combined with other factors.
Area of Science:
- Immunology
- Dermatology
- Genetics
Background:
- Integrin alpha(E)beta(7) is crucial for mucosal T lymphocyte localization.
- Its role in cutaneous T lymphocytes was previously unclear.
- Alpha(E) deficiency was unexpectedly linked to skin inflammation.
Purpose of the Study:
- Investigate the role of integrin alpha(E)beta(7) in skin inflammation.
- Determine if alpha(E) deficiency contributes to inflammatory skin disease.
- Explore the interplay of genetic and environmental factors in alpha(E)-related skin pathology.
Main Methods:
- Studied alpha(E)-deficient mice (alpha(E)(-/-)) on mixed genetic backgrounds.
- Analyzed skin lesions for immune cell infiltration and cytokine expression.
- Utilized adoptive transfer of splenocytes and T cells into immunodeficient mice (scid/scid).
- Examined a murine model of hyperproliferative inflammatory skin disorder.
Main Results:
- Alpha(E) deficiency correlated with inflammatory skin lesions in specific mouse models.
- Lesions showed CD4(+) T cell and neutrophil infiltration with elevated inflammatory cytokines.
- Transfer of alpha(E)(-/-) splenocytes induced skin inflammation in scid/scid mice.
- Alpha(E)-deficient T cells exacerbated skin lesions in a murine model.
Conclusions:
- Integrin alpha(E)beta(7) deficiency is associated with inflammatory skin disease.
- The development of skin lesions involves immune dysregulation and is influenced by genetic and environmental factors.
- Alpha(E)-expressing cells play a protective role in cutaneous inflammation.
