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Release of lymphokines after infection with epstein barr virus in vitro ii. a monocyte dependent inhibitor of interleukin 1 downregulates the production of interleukin 2 and interferon gamma in rheumatoid arthritis



Release of lymphokines after infection with epstein barr virus in vitro ii. a monocyte dependent inhibitor of interleukin 1 downregulates the production of interleukin 2 and interferon gamma in rheumatoid arthritis



Journal of Immunology 136(10): 3643-3648



Epstein Barr virus (EBV)-infection of normal peripheral blood mononuclear cells (PBMC) in vitro induces IFN-.alpha. secretion from B cell and natural killer (NK) cell populations, and IFN-.gamma. secretion from T cells. IFN-.gamma. depends on prior elaboration of IL 2 and IL 1 that originates from monocytes and NK cells. PBMC from rheumatoid arthritis (RA) patients released moderately elevated levels of IFN-.alpha. (236 .+-. 62 U/ml vs 168 .+-. 34 in normals). In contrast, IFN-.gamma. was significantly lower in RA (88 .+-. 34 U/ml vs 209 .+-. 32) with an associated deficit in IL 2. A monocyte-dependent factor was shown to be responsible for this deficit, since monocyte depletion of RA cultures normalized the levels of IL 2 and IFN-.gamma. Significantly lower levels of IL 1 activity were present in the supernatants of RA PBMC cultures as compared with normal cultures, and this was shown to be associated with presence of a nondialyzable IL 1 inhibitor. This inhibitor was capable of preventing the IL 1-dependent synthesis of IL 2 and IFN-.gamma. by normal PBMC. Exogenous IL 1 or IL 2 restored the deficient IFN-.gamma. secretion in RA PBMC. Thus, the deficient ability of RA lymphocytes to control EBV infection may be secondary to impairment of a monocyte-T cell interaction at the level of IL 1.

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Accession: 006306086

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PMID: 3009609



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