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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4⁺CD45RB^high T Cells into Immunodeficient Mice

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.

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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.