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Despite strong evidence supporting a pathway of human T cell differentiation characterized by changes in the expression of CCR7, CD28, CD27 and CD62L, few studies have addressed the mechanisms of pathway regulation. Cutaneous lymphocyte-associated antigen (CLA)-positive skin-homing CD8(+) T cells expressed significantly elevated levels of activation markers compared with CLA(-) CD8(+) T cells in individuals (n = 27) with cutaneous atopic disease. Despite such an activated phenotype, CLA(+) T cells expressed significantly higher levels of CCR7 than a CLA(-) T cell subset. Interleukin (IL)-4 was found to dramatically promote CCR7 expression by antigen-specific CD8(+) cells. Furthermore, skin-homing CD8(+) T cells from individuals with severe disease produced significantly less IL-10 than those derived from mildly affected atopic subjects. Thus in a T-helper 2 dominated disease, tissue-specific CD8(+) T cells show altered CCR7 expression and cytokine production, which may contribute to continued lymph node homing, antigen presentation and disease. IL-4 promotes expression of CCR7, a marker linked to existing models of CD8(+) T cell differentiation.

Original publication

DOI

10.1111/j.1365-2567.2006.02478.x

Type

Journal article

Journal

Immunology

Publication Date

01/2007

Volume

120

Pages

66 - 72

Keywords

CD8-Positive T-Lymphocytes, Cell Differentiation, Cell Movement, Cells, Cultured, Cytokines, Dermatitis, Atopic, Dose-Response Relationship, Immunologic, Humans, Interleukin-4, Interleukins, Lymphocyte Activation, Receptors, CCR7, Receptors, Chemokine, Skin, Th2 Cells