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IL-12 Enhances CTL Synapse Formation and Induces Self-Reactivity¹

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

Immunological synapse formation between T cells and target cells can affect the functional outcome of TCR ligation by a given MHC-peptide complex. Although synapse formation is usually induced by TCR signaling, it is not clear whether other factors can affect the efficiency of synapse formation. Here, we tested whether cytokines could influence synapse formation between murine CTLs and target cells. We found that IL-12 enhanced synapse formation, whereas TGFβ decreased synapse formation. The enhanced synapse formation induced by IL-12 appeared to be functional, given that IL-12-treated cells could respond to weak peptides, including self-peptides, to which the T cells were normally unresponsive. These responses correlated with expression of functionally higher avidity LFA-1 on IL-12-treated CTLs. These findings have implications for the function of IL-12 in T cell-mediated autoimmunity.

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 partially supported by the American Cancer Society (to M.A.M.).

² Address correspondence and reprint requests to Dr. Andrey S. Shaw, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110. E-mail address: shaw{at}pathology.wustl.edu

³ Abbreviations used in this paper: cSMAC, central supramolecular activation cluster; pSMAC, peripheral supramolecular activation cluster; rmIL-12, recombinant mouse IL-12; Treg, regulatory T cell.

⁴ The online version of this article contains supplemental material.

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