IL‐4 augments anisomycin‐induced p38 activation via Akt pathway in a follicular dendritic cell (FDC)‐like line

FEBS Letters

Park, Sun-Mi¹  Jin, Hyung-Sung¹  Park, Jae-Won¹  Lee, Tae H.¹  Jeon, Hye-Kyung¹  Lee, Hyang-Mi¹ 

[1] Department of Biology and Protein Network Research Center, Yonsei University, 134 Shinchon-dong, Seodaemoon-gu, Seoul 120-749, South Korea

关键词: IL-4;    Akt;    p38;    Follicular dendritic cell;    FDC;    follicular dendritic cell;    GC;    germinal center;    ERK;    extracellular signal-regulated kinase;    PI3K;    phosphatidylinositol-3′-kinase;    MAPK;    mitogen-activated protein kinase;    MKK;    MAPK kinase;    MEK;    MAPK/ERK kinase;    MEKK;    MEK kinase;   

DOI  :  10.1016/S0014-5793(03)00800-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Follicular dendritic cells (FDCs) play pivotal roles in germinal center (GC) responses in secondary lymphoid follicles, and their functions are influenced by cytokines present in the GC. We investigated the functional effects of interleukin-4 (IL-4) using an established FDC-like line of HK cells. In spite of the activation of ERK1/2 and PI3K/Akt pathways by IL-4, which are implicated in the induction of cell proliferation and survival, IL-4 did not exhibit protective function on anisomycin-induced apoptosis of HK cells, but rather slightly enhanced it. This IL-4 effect correlated with the up-regulation of anisomycin-induced p38 signaling, which is attenuated by inhibition of the PI3K/Akt pathway. Expression of an active form of Akt increased anisomycin-elicited activation of p38 and its upstream kinase MKK3/6. Our data indicate a positive cross-talk between the p38 and PI3K/Akt pathways.

【 授权许可】

Unknown