期刊
IMMUNOLOGICAL REVIEWS
卷 192, 期 1, 页码 131-142出版社
WILEY
DOI: 10.1034/j.1600-065X.2003.00019.x
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- NCRR NIH HHS [RR15557] Funding Source: Medline
- NIAID NIH HHS [AI51454, AI42138, AI45666] Funding Source: Medline
The c-Jun aminoterminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase signaling pathways have been associated with cell death, differentiation and proliferation. CD4(+) and CD8(+) T cells have different effector functions after antigen stimulation and control specific aspects of the immune response. The studies carried out in our group indicate that the role of JNK and p38 MAP kinases in CD4(+) T cells is different from their role in CD8(+) T cells. Moreover, these two pathways are not redundant in either T cell population. We have also shown that p38 MAP kinase regulates early stages of T cell development in the thymus. It is therefore important to consider the specific function of these kinases in each T cell population when pharmacological inhibitors of JNK and p38 MAP kinases are used for therapeutic purposes to control the immune response.
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