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Migration of Tissue Dendritic cells in Immune‐mediated Inflammatory Diseases: Role of Cooperative Interaction Between Epidermal gd T Cells and Skin Dendritic Cells
Author(s) -
Eriksson Anna Ulrika,
Singh Ram Raj
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.668.13
Subject(s) - epidermis (zoology) , inflammation , immune system , immunology , cd1d , microbiology and biotechnology , dendritic cell , antigen , biology , lymph node , in vivo , natural killer t cell , t cell , anatomy
The skin‐resident dendritic cells (DC), namely dermal DC (dDC) and Langerhans cells (LC), are believed to sample antigens in the skin and migrate to cutaneous lymph nodes (CLN) to induce immunity or tolerance to these antigens. We report a previously unappreciated defect in the migration of LC prior to the appearance of skin inflammation in genetically autoimmune‐prone MRL‐Fas lpr/lpr and MRL‐Fas +/+ mice. In these mice, LC displays a drastic reduction in migration in the steady state as well as upon in vitro or in vivo stimulation. This defect is associated with markedly reduced numbers of γδ dendritic epidermal T cells (DETC) in the epidermis of MRL mice. The role of DETC is not fully investigated but they are believed to be involved in homeostasis of skin, and facilitate wound healing. Both defects are corrected and skin inflammation is reduced by in vivo treatment of these animals with α‐galactosylceramide, a glycolipid that binds CD1d and activates natural killer T (NKT) cells. Surprisingly, DETC numbers and LC migration are also reduced in CD1d‐deficient, but not in NKT cell‐deficient, mice. These data suggest that a glycolipid can induce expansion of skin γδ DETC, which promote the migration of LC from epidermis to skin draining lymph node.