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Department of Dermatology, Hamamatsu University School of Medicine, Higashi-ku, Hamamatsu, Japan
Gold compounds clinically used as immunomodulators have high potential to evoke hypersensitivity reactions as an adverse effect. To explore the mechanism of gold allergy, we immunologically characterized T cells infiltrating skin rashes and generated 44 gold-specific T cell clones and lines from a rheumatoid arthritis patient who developed skin rashes and systemic symptoms after gold treatment. CD4+ and CD8+ cells predominantly infiltrating the skin rashes and some of the T cell clones and lines shared common Vβs. These cells exhibited Th0-like, Th2-like, and Tc1-like cytokine profiles, and showed chemotactic activities for thymus and activation-regulated chemokine and IFN-
-inducible protein-10 corresponding to the cytokine profiles. T cell recognition of gold consisted of MHC-restricted and MHC-independent pathways. Blocking studies with anti-MHC Abs indicated that the groove of MHC in APCs, where Ags should ordinarily be settled, did not serve as a conjugating site of gold for these T cells in certain cases. These observations raise the possibility that gold-specific CD4+ and CD8+ T cells and APCs promiscuously interact under stimulation with gold, resulting in various clinical manifestations in gold allergy.
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1 This work was partly supported by a Grant-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (17591168).
2 Address correspondence and reprint requests to Dr. Hideo Hashizume, Department of Dermatology, Hamamatsu University School of Medicine, 1-20-1 Handa-yama, Higashi-ku, Hamamatsu 431-3192, Japan. E-mail address: hihashiz{at}hama-med.ac.jp
3 Abbreviations used in this paper: RA, rheumatoid arthritis; CBA, cytometric bead array; FCM, flow cytometry; IP-10, IFN-
-inducible protein-10; LCL, lymphoblastoid B cell line; TARC, thymus and activation-regulated chemokine; TCC, T cell clone; TCL, T cell line.
4 The online version of this article contains supplemental material.
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