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CD8 T Cells Producing IL-17 and IFN- Initiate the Innate Immune Response Required for Responses to Antigen Skin Challenge¹

Danielle D. Kish^2,*, Xiaoxia Li^*, and Robert L. Fairchild^*,,

^* Department of Immunology and Glickman Urological Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, and Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106

Effector CD8 T cell recruitment into the skin in response to Ag challenge requires prior CXCL1/KC-directed neutrophil infiltration. Mechanisms inducing CXCL1 production and the dynamics of neutrophil-CD8 T cell interactions during elicitation of Ag-specific responses in the skin were investigated. CXCL1 and CXCL2/MIP-2 were produced within 3–6 h of Ag challenge at 10-fold higher levels in skin challenge sites of Ag-sensitized vs nonsensitized mice. In the challenge sites of sensitized mice this production decreased at 6–9 h postchallenge to near the levels observed in skin challenge sites of nonsensitized mice but rose to a second peak 12 h after challenge. The elevated early neutrophil chemoattractant production at 3–6 h after skin challenge of sensitized animals required both IFN- and IL-17, produced by distinct populations of Ag-primed CD8 T cells in response to Ag challenge. Although induced by the Ag-primed CD8 T cells, the early CXCL1 and CXCL2 production was accompanied by neutrophil but not CD8 T cell infiltration into the skin Ag challenge site. Infiltration of the CD8 T cells into the challenge site was not observed until 18–24 h after challenge. These results demonstrate an intricate series of early interactions between Ag-specific and innate immune components that regulate the sequential infiltration of neutrophils and then effector T cells into the skin to mediate an immune response.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants R01 AI45888 from the National Institute of Allergy and Infectious Diseases.

² Address correspondence and reprint requests to: Danielle D. Kish, NB3-30, Department of Immunology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195-0001. E-mail address: kishd{at}ccf.org

³ Abbreviations used in this paper: CHS, contact hypersensitivity; DNFB, 2,4-dinitro-1-fluorobenzene; LNC, lymph node cell.