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ENDOTHELIAL CELL PRESENTATION OF ANTIGEN INITIATES THE ADAPTIVE‐INNATE IMMUNE INTERACTION SEQUENCES IN T CELL MEDIATED RESPONSES IN THE SKIN
Author(s) -
Kish Danielle D.,
Fairchild Robert L.
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.664.10
Subject(s) - t cell , cd8 , immunology , sensitization , chemistry , hapten , cytotoxic t cell , cytokine , immune system , antigen , microbiology and biotechnology , biology , in vitro , biochemistry
Contact hypersensitivity (CHS) is a CD8 T cell‐mediated response to skin sensitization and challenge with hapten. Hapten‐primed CD8 T cell recruitment into the challenged skin to mediate CHS requires prior CXCL1/KC and CXCL2/MIP‐2 directed neutrophil infiltration. The factors inducing KC and MIP‐2 to challenge were investigated. KC and MIP‐2 were produced 3–6 h after challenge with dinitrofluorobenzene (DNFB) in sensitized, but not unsensitized, mice and were dependent on hapten‐specific CD8 T cells. KC and MIP‐2 production was accompanied by expression of IFN‐g and IL‐17. DNFB sensitization induced hapten‐specific CD8 T cells producing IFN‐g and IL‐17. CHS responses and KC production were at naïve levels in sensitized and challenged IFN‐γ −/− and IL‐17 −/− mice. DNFB‐induced KC in naïve mice was restored by co‐transfer of CD8 T cells from sensitized IFN‐γ −/− and IL‐17 −/− mice but not each population alone. In vitro, primed CD8 T cells stimulated hapten‐labeled EC to produce KC which was blocked by either anti‐IFN‐γ or anti‐IL‐17 mAb. Addition of rIFN‐γ and rIL‐17 synergized to stimulate EC to produce KC. These results indicate that hapten sensitization induces populations of CD8 T cells producing IFN‐γ and IL‐17. Activation of both T cell populations is required to induce EC in the challenge site to produce KC and MIP‐2 to initiate elicitation of the CHS response.