Regulation of T cells and cytokines by the interleukin-10 (IL-10)-family cytokines IL-19, IL-20, IL-22, IL-24 and IL-26.

Oral H. B., Kotenko S., YILMAZ M., Mani O., Zumkehr J., Blaser K., ...Daha Fazla

European journal of immunology, cilt.36, sa.2, ss.380-8, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 36 Sayı: 2
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1002/eji.200425523
  • Dergi Adı: European journal of immunology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.380-8
  • Anahtar Kelimeler: interleukin-10, new cytokines, T cells, DIFFERENTIATION-ASSOCIATED GENE, INDUCIBLE FACTOR, CUTTING EDGE, MELANOMA DIFFERENTIATION, RECEPTOR COMPLEXES, STAT ACTIVATION, TYPE-1 CELLS, IFN-GAMMA, TGF-BETA, IL-TIF
  • Bursa Uludağ Üniversitesi Adresli: Evet

Özet

The family of IL-10-related cytokines includes several human members, IL-19, IL-20, IL-22, IL-24 and IL-26, and a series of herpesviral and poxviral paralogs. Some of these cytokines share common receptor subunits. In this study, we investigated the effects of these cytokines on naive T cell differentiation, antigen-specific T cell suppression, survival and expression of surface markers in comparison to IL-10 and cytomegalovirus (CMV)-IL-10. Human CD45RA(+) T cells were stimulated in the presence of IL-10-family cytokines in sequential 12-day cycles. After three to four cycles of stimulation, IL-10 and CMV-IL-10 led to increased IFN-gamma and IL-10 but decreased IL-4 and IL-13. Interestingly, long-term exposure of T cells to IL-19, IL-20 and IL-22 down-regulated IFN-gamma but up-regulated IL-4 and IL-13 in T cells and supported the polarization of naive T cells toTh2-like cells. in contrast, neutralization of endogenous IL-22 activity by IL-22-binding protein decreased IL-4, IL-13 and IFN-gamma synthesis. The antigen-specific suppressor activity of IL-10 and CMV-IL-10 was not observed for any of the other IL-10-family cytokines. These data demonstrate that IL-19, IL-20 and IL-22 may participate in T cell-mediated diseases by distinct regulation of T cell cytokine profiles.