Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression.
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- R de Waal Malefyt
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- J Haanen
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- H Spits
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- M G Roncarolo
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- A te Velde
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- C Figdor
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- K Johnson
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- R Kastelein
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- H Yssel
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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- J E de Vries
- DNAX Research Institute, Human Immunology, Palo Alto, California 94304.
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抄録
<jats:p>Interleukin 10 (IL-10) and viral IL-10 (v-IL-10) strongly reduced antigen-specific proliferation of human T cells and CD4+ T cell clones when monocytes were used as antigen-presenting cells. In contrast, IL-10 and v-IL-10 did not affect the proliferative responses to antigens presented by autologous Epstein-Barr virus-lymphoblastoid cell line (EBV-LCL). Inhibition of antigen-specific T cell responses was associated with downregulation of constitutive, as well as interferon gamma- or IL-4-induced, class II MHC expression on monocytes by IL-10 and v-IL-10, resulting in the reduction in antigen-presenting capacity of these cells. In contrast, IL-10 and v-IL-10 had no effect on class II major histocompatibility complex (MHC) expression on EBV-LCL. The reduced antigen-presenting capacity of monocytes correlated with a decreased capacity to mobilize intracellular Ca2+ in the responder T cell clones. The diminished antigen-presenting capacities of monocytes were not due to inhibitory effects of IL-10 and v-IL-10 on antigen processing, since the proliferative T cell responses to antigenic peptides, which did not require processing, were equally well inhibited. Furthermore, the inhibitory effects of IL-10 and v-IL-10 on antigen-specific proliferative T cell responses could not be neutralized by exogenous IL-2 or IL-4. Although IL-10 and v-IL-10 suppressed IL-1 alpha, IL-1 beta, tumor necrosis factor alpha (TNF-alpha), and IL-6 production by monocytes, it was excluded that these cytokines played a role in antigen-specific T cell proliferation, since normal antigen-specific responses were observed in the presence of neutralizing anti-IL-1, -IL-6, and -TNF-alpha mAbs. Furthermore, addition of saturating concentrations of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha to the cultures had no effect on the reduced proliferative T cell responses in the presence of IL-10, or v-IL-10. Collectively, our data indicate that IL-10 and v-IL-10 can completely prevent antigen-specific T cell proliferation by inhibition of the antigen-presenting capacity of monocytes through downregulation of class II MHC antigens on monocytes.</jats:p>
収録刊行物
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- The Journal of experimental medicine
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The Journal of experimental medicine 174 (4), 915-924, 1991-10-01
Rockefeller University Press
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詳細情報 詳細情報について
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- CRID
- 1363388843677771008
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- NII論文ID
- 30017430043
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- NII書誌ID
- AA00697559
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- ISSN
- 15409538
- 00221007
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