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Abnormal lymphocyte reactivity to self-major histocompatibility antigens in rheumatoid arthritis.

作者信息

Kingsley G H, Pitzalis C, Panayi G S

机构信息

Rheumatology Unit, United Medical School, Guy's Hospital, London, England.

出版信息

J Rheumatol. 1987 Aug;14(4):667-73.

PMID:2959772
Abstract

Proliferation of rheumatoid and control peripheral blood mononuclear cells to OKT3, phorbol myristic acid (PMA), phytohemagglutinin (PHA), tuberculin PPD and in the autologous mixed lymphocyte reaction (AMLR) was investigated. Only the responses to PPD and in the AMLR were depressed. This was not due to suppression by OKT8 lymphocytes. The proportion of antigen responsive (T4+ 4B4+) cells was normal but suppressor-inducer (T4+ 2H4+) cells were decreased. The depressed response was not completely restored by addition of recombinant interleukin-2. We propose that a basic defect in rheumatoid arthritis resides in T lymphocytes which react to self-major histocompatibility complex antigens either on their own, as in the AMLR, or as restriction elements in the presentations of soluble antigen.

摘要

相似文献

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Abnormal lymphocyte reactivity to self-major histocompatibility antigens in rheumatoid arthritis.
J Rheumatol. 1987 Aug;14(4):667-73.
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