期刊
IMMUNOLOGY
卷 132, 期 1, 页码 104-110出版社
WILEY
DOI: 10.1111/j.1365-2567.2010.03345.x
关键词
autoimmunity; human; inflammation; rheumatoid arthritis; T cells
类别
资金
- ARC
P>Peripheral blood CD4+ CD45RO+ T cells activated in vitro are able to induce expression of tumour necrosis factor-alpha (TNF-alpha) in monocytes via a contact-dependent mechanism. Activation is achieved either with interleukin-2 (IL-2)/IL-6/TNF-alpha over an 8-day period or cross-linking CD3 using anti-CD3 antibody for 48 hr. In this paper, we show that the p38 mitogen-activated protein kinase (MAPK) signalling pathway played different roles in the generation of effector function in these two types of activated T cells. In anti-CD3 activated T cells, p38 MAPK is a negative regulator for anti-CD3 induced cell proliferation and has no significant effect on the acquisition of either the effector function (induction of monocyte-derived TNF-alpha) or production of T-cell cytokines. In contrast, the p38 MAPK signalling pathway is required for the acquisition of cytokine-induced effector function and promotes cell proliferation and cytokine production.
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