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Passive Transfer of Experimental Autoimmune Neuritis by IL‐12 and IL‐18 Synergistically Potentiated Lymphoid Cells is Regulated by NKR‐P1+ Cells
Author(s) -
Sun B.,
Li H.L.,
Wang J.H.,
Wang G.Y.,
Zhao R.,
Mu L.L.,
Jin L.H.
Publication year - 2007
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2007.01922.x
Subject(s) - immunology , interleukin 12 , interleukin 21 , interleukin , cell , interleukin 4 , chemistry , biology , medicine , t cell , cytokine , in vitro , immune system , cytotoxic t cell , biochemistry
The aim of this study was to investigate the roles and mechanism of interleukin‐12 (IL‐12) and interleukin‐18 (IL‐18) in potentiating the autoreactivity of lymphoid cells specific for P2 53–78 peptide. P2 53–78‐specific lymphoid cells in the presence of IL‐12 or IL‐18 alone passive transferred only moderate experimental autoimmune neuritis (EAN) into a low percentage of recipients. However, lymphoid cells co‐cultured with both cytokines transferred aggressive clinical and histological EAN into all recipients. NKR‐P1+ cells (including NK and NKT cells) played an immunosuppressive function in passive transfer EAN and depletion of NKR‐P1+ cells by anti‐NKR‐P1 Ab and complement induced a more serious form of EAN. Nevertheless, lymphoid cells co‐cultured with both IL‐12 and IL‐18 induced high levels of interferon‐ γ (IFN‐ γ ) and promoted Th1 differentiation partially through NKR‐P1+ cells and to some extent, NKR‐P1+ cell depletion inhibited the auto‐reactivity of lymphoid cells treated with IL‐12 and IL‐18.