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Epstein-Barr virus-induced gene-3 (EBI-3) associates with p28 to form interleukin-27 (IL-27) or with IL-12p35 to form IL-35. Both IL-27 and IL-35 have immunosuppressive functions and especially IL-35 has been implicated in the suppressive function of regulatory T cells (Treg). To address the role of EBI-3 in immune regulation, delayed-type hypersensitivity (DTH) responses were examined in EBI-3-deficient (EBI-3(-/-)) mice. EBI-3(-/-) mice developed deteriorated DTH responses as shown by the enhanced footpad swelling and augmented infiltration of inflammatory cells into the antigen-challenged footpads as compared with wild-type (WT) mice. While EBI-3-deficiency showed little effects on antigen-specific IFN-gamma production of lymph node cells, IL-17 production was drastically augmented in EBI-3(-/-) cells as compared with in WT cells. In addition, reduced IL-10 production was also evident in EBI-3(-/-) CD4(+) T cells. Interestingly, the development and suppressive function of Treg to inhibit effector T cell proliferation was not affected by EBI-3-deficiency. These data clearly demonstrated the immunosuppressive function of EBI-3 and provided complementary evidence that EBI-3 and EBI-3-containing cytokines might be taken into consideration as potential targets for some immune-related diseases.

Original publication

DOI

10.1016/j.imlet.2010.01.001

Type

Journal article

Journal

Immunol Lett

Publication Date

16/02/2010

Volume

128

Pages

108 - 115

Keywords

Animals, Cytokines, Disease Models, Animal, Female, Foot, Herpesvirus 4, Human, Humans, Hypersensitivity, Delayed, Immunosuppression, Lymph Nodes, Male, Mice, Mice, Inbred C57BL, Minor Histocompatibility Antigens, Receptors, Cytokine, Serum Albumin, Bovine, T-Lymphocytes, T-Lymphocytes, Regulatory