Abstract
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-γ 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 language | English |
|---|---|
| Pages (from-to) | 108-115 |
| Number of pages | 8 |
| Journal | Immunology Letters |
| Volume | 128 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 1 2010 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology
Cite this
Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice. / Tong, Honglian; Miyazaki, Yoshiyuki; Yamazaki, Masanori; Hara, Hiromitsu; Waldmann, Herman; Hori, Shohei; Yoshida, Hiroki.
In: Immunology Letters, Vol. 128, No. 2, 01.02.2010, p. 108-115.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice
AU - Tong, Honglian
AU - Miyazaki, Yoshiyuki
AU - Yamazaki, Masanori
AU - Hara, Hiromitsu
AU - Waldmann, Herman
AU - Hori, Shohei
AU - Yoshida, Hiroki
PY - 2010/2/1
Y1 - 2010/2/1
N2 - 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-γ 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.
AB - 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-γ 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=77249097317&partnerID=8YFLogxK
U2 - 10.1016/j.imlet.2010.01.001
DO - 10.1016/j.imlet.2010.01.001
M3 - Article
C2 - 20064562
AN - SCOPUS:77249097317
VL - 128
SP - 108
EP - 115
JO - Immunology Letters
JF - Immunology Letters
SN - 0165-2478
IS - 2
ER -