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Sj HSP 60 induces CD 4 + CD 25 + Foxp3 + Tregs via TLR 4‐Mal‐drived production of TGF ‐β in macrophages
Author(s) -
Zhou Sha,
Qi Qianqian,
Wang Xiaofan,
Zhang Lina,
Xu Lei,
Dong Liyang,
Zhu Jifeng,
Li Yalin,
Wang Xuefeng,
Xu Zhipeng,
Liu Feng,
Hu Wei,
Zhou Liang,
Chen Xiaojun,
Su Chuan
Publication year - 2018
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.12160
Subject(s) - foxp3 , antigen , transforming growth factor beta , transforming growth factor , immune system , heat shock protein , transcription factor , chemistry , biology , microbiology and biotechnology , immunology , biochemistry , gene
CD 4 + CD 25 + Foxp3 + regulatory T cells (Tregs) play a pivotal role in limiting immunopathological damage to host organs after schistosome infection. Transforming growth factor‐β ( TGF ‐β) is an essential factor for the periphery conversion of CD 4 + CD 25 − T cells into CD 4 + CD 25 + Foxp3 + Tregs by inducing the key transcription factor Foxp3. Antigen presenting cells ( APC s), which highly express TGF ‐β, are involved in parasite antigen‐induced Treg conversion in peripheral. However, the mechanisms underlying high TGF ‐β induction in APC s by parasite antigens remain to be clarified during schistosome infection. Here, we demonstrated that Schistosoma japonicum stress protein, heat shock protein 60 (Sj HSP 60), promoted TGF ‐β production in macrophages (Mφ). Furthermore, we showed that activation of TLR 4‐Mal (MyD88 adaptor‐like protein) signaling by Sj HSP 60 is necessary for induction of TGF ‐β expression in Mφ, which subsequently promoted Treg induction. Our results not only demonstrate a novel mechanism of TGF ‐β production in Mφ for inducing Tregs in mice with schistosomiasis, but also allude to the possibility of targeting parasite stress protein for potential therapeutics.