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The Journal of Immunology, 2001, 167: 6884-6892.
Copyright © 2001 by The American Association of Immunologists

Differential IL-10R1 Expression Plays a Critical Role in IL-10-Mediated Immune Regulation1

Yaozhong Ding*, Lihui Qin*, Dmitriy Zamarin*, Sergei V. Kotenko{dagger}, Sidney Pestka{dagger}, Kevin W. Moore{ddagger} and Jonathan S. Bromberg2,*

* Institute for Gene Therapy and Molecular Medicine, Mount Sinai School of Medicine, New York, NY 10029; {dagger} Department of Molecular Genetics and Microbiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854; and {ddagger} Department of Molecular Biology, DNAX Research Institute, Palo Alto, CA 94304

In this study, we characterized the differential receptor-binding specificity, affinity, and Janus kinase-STAT activation of cellular IL-10 (cIL-10) compared with viral IL-10 (vIL-10). Only cells expressing IL-10R1 bind human IL-10 or vIL-10. IL-10R2 does not bind to cIL-10 or vIL-10 alone and its presence does not enhance the receptor-binding affinity of cIL-10 or vIL-10, but it is essential for both cIL-10- and vIL-10-mediated signal transduction and immune regulation. Responses initiated by cIL-10 and vIL-10 were compared in B cell and mast cell lines, and demonstrated that the inability of vIL-10 to stimulate immune responses, as compared with human IL-10, is due to failure to initiate signaling. Absent signal transduction is due to low level expression of cell surface IL-10R1, since overexpressing IL-10R1 allows vIL-10 to initiate cIL-10-like signals and subsequent biological responses. These results are similar in primary cells, since splenocytes respond to both cIL-10 and vIL-10, while thymocytes respond only to cIL-10 and have very low mouse IL-10R1 but not mouse IL-10R2 expression. These data demonstrate that IL-10R1 expression plays a critical role in determining whether cells respond to IL-10. Modulation of cell surface IL-10R1 density might be an important mechanism for determining whether IL-10 leads to immunostimulation or immunosuppression in vivo.




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