Premium
IL‐4 augments anisomycin‐induced p38 activation via Akt pathway in a follicular dendritic cell (FDC)‐like line
Author(s) -
Lee Hyang-Mi,
Jin Hyung-Sung,
Park Jae-Won,
Park Sun-Mi,
Jeon Hye-Kyung,
Lee Tae H.
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00800-7
Subject(s) - anisomycin , pi3k/akt/mtor pathway , protein kinase b , germinal center , microbiology and biotechnology , p38 mitogen activated protein kinases , follicular dendritic cells , chemistry , signal transduction , apoptosis , cancer research , biology , kinase , t cell , immunology , b cell , mapk/erk pathway , immune system , antigen presenting cell , biochemistry , antibody
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.