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Attenuation of contact hypersensitivity by cell‐permeable heat shock protein 70 in BALB /c mouse model
Author(s) -
Park Jin Mo,
Je Jeong Hwan,
Wu Wen Hao,
Jee Hyun Joong,
Lee SangKyou,
Lee MinGeol
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12044
Subject(s) - chemistry , hsp70 , foxp3 , heat shock protein , il 2 receptor , tumor necrosis factor alpha , t cell , mapk/erk pathway , immune system , microbiology and biotechnology , signal transduction , immunology , biology , biochemistry , gene
In contact hypersensitivity ( CHS ), multiple cells, inflammatory mediators and cytokines are known to be involved in the regulation of the immune response. Previously, we revealed the reactive oxygen species generation by 2, 4, 6‐trinitrobenzene sulphonic acid ( TNBS ) in vivo , followed by heat shock protein 70 (Hsp70) carbonylation and the exogenous antioxidant role of cell‐permeable Hsp70. Here, we demonstrate the role of Hsp70 using cell‐permeable Hsp70 in the mouse CHS model. Pretreatment of cell‐permeable Hsp70: (i) suppressed ear swelling; (ii) down‐regulated phosphorylated p38, but up‐regulated phosphorylated extracellular signal‐regulated kinase; (iii) increased population of CD 4 + CD 25 + Foxp3 + T cells; (iv) decreased secretion of tumor necrosis factor‐α ( TNF ‐α), IL ‐12, interferon‐γ and IL ‐2 and (v) but up‐regulated IL ‐4 and transforming growth factor beta ( TGF ‐β) in the lymph nodes. In conclusion, cell‐permeable Hsp70 attenuates CHS through modulation of MAPK pathway and regulation of Th1, Th2 and regulatory T cells.