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Induction of regulatory T cells by Opisthorchis viverrini
Author(s) -
Kaewraemruaen C.,
Sermswan R. W.,
Wongratanacheewin S.
Publication year - 2016
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12358
Subject(s) - opisthorchis viverrini , biology , opisthorchiasis , foxp3 , immunology , il 2 receptor , opisthorchis , t cell , immune system , clone (java method) , antigen , t lymphocyte , spleen , mesenteric lymph nodes , medicine , liver fluke , gene , helminths , biochemistry
Summary Opisthorchis viverrini causes public health problems in South‐East Asia. Recently, TGF ‐β and IL ‐10 have been reported to increase in O. viverrini ‐infected hamsters but the sources of these cytokines are still unknown. In this study, the CD 4 + T cells in infected hamsters were investigated. It was demonstrated that IL ‐4 + CD 4 + T cells were significantly increased in hamster spleens and mesenteric lymph nodes ( MLN s) during chronic infection. Interestingly, IL ‐10 + CD 4 + T cells were also discovered at a significant level while Treg (T regulatory)‐like TGF ‐ β + CD 4 + T cells were in MLN s of infected hamsters. Moreover, the CD 4 + CD 25 + Foxp3 + Treg cell response was significantly found both in spleens and MLN s in infected hamsters. The findings were then confirmed by development of T‐cell clones against crude somatic antigens ( CSA g) in immunized BALB /c mice. Five clones named TCC 21, TCC 23, TCC 35, TCC 41 and TCC 108 were established. The TCC 21 was found to be the TGF ‐β + CD 4 + while TCC 35, TCC 41 and TCC 108 were IL ‐4 + CD 4 + and TCC 23 was IFN ‐γ + CD 4 + . This TGF ‐β + CD 4 + T clone showed an inhibitory function in vitro in mononuclear cell proliferation via TGF ‐β‐mediated mechanisms. This study indicated that O. viverrini ‐infected hamsters could induce TGF ‐β + CD 4 + Treg‐like cells. The CSA g‐specific Tregs secreted high TGF ‐β, and limited immune cell proliferation.