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International Immunology, Vol. 12, No. 1, 103-112, January 2000
© 2000 Japanese Society for Immunology

IL-12 is produced by antigen-presenting cells stimulated with soluble {alpha}ß TCR and restores impaired Th1 responses

Keiko Kawamoto, Vipin Paliwal1, Rajani Ramabhadran1, Marian Szczepanik2, Ryohei F. Tsuji3, Hiroshi Matsuda4 and Philip W. Askenase1

Department of Veterinary Surgery, College of Agriculture, University of Osaka Prefecture, Sakai, Osaka 593, Japan
1 Section of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8013, USA
2 Department of Immunology, Jagiellonian University College of Medicine, 31–121, Krakow, Poland
3 Noda Institute for Scientific Research, 399 Noda, Noda-shi, Chiba-ken 278, Japan
4 Faculty of Veterinary Clinic, Department of Agriculture, Tokyo University of Agriculture and Technology, 3-8-5 Saiwai-cho, Fuchu, Tokyo 183, Japan

Correspondence to: P. W. Askenase

Contact sensitivity (CS) is a cutaneous Th1 response that is induced by skin painting with reactive hapten. In prior in vivo studies of CS, we showed that recombinant soluble {alpha}ßTCR (sTCR) acted non-specifically to protect CS-effector T cells from suppression, but no molecular mechanism was determined. In the current study, we employed an in vitro system to investigate the mechanism of how sTCR protect CS-effector T cells from suppression. Immune CS-effector cells and appropriate hapten-conjugated antigen-presenting cells (APC) were incubated together with down-regulatory culture supernatant produced by suppressive spleen cells from mice tolerized i.v. with specific hapten, which produced strong inhibition of IFN-{gamma} production by the CS-effector cells. Importantly, addition of two different sTCR, of unrelated specificity, reversed this down-regulation and thus restored IFN-{gamma} production. We found that the APC, and not the CS-effector T cells, were the locus of the sTCR-mediated protection and showed direct binding of sTCR to APC by flow cytometry. Further, addition of anti-IL-12 showed that sTCR protection was due to IL-12 induced by sTCR and released by the APC, and was confirmed by ELISA measurement of IL-12 induced in APC supernatants by sTCR incubation. These results indicated a possible new regulatory loop in which suppression was reversed by IL-12 derived from APC, following direct surface binding of sTCR, and enhanced by IFN-{gamma} production from the Th1 CS-effector cells.

Keywords: T cell suppression, delayed-type hypersensitivity, contact sensitivity

Transmitting editor: K. Okumura


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