期刊
JOURNAL OF IMMUNOLOGY
卷 183, 期 1, 页码 172-180出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0802325
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资金
- National Institutes of Health [AI053703, ES09098, AI058300, DA016545, HL058641, P01AT003961]
CD4 T cells can be primarily polarized to differentiate into Th1 or Th2 cells. CD44 is a marker of T cell activation and a property of long-lived memory cells and implicated in cell migration, activation, and differentiation. To date, whether CD44 has a role in regulating Th1-Th2 differentiation has not been determined. In this study, we compared Th1 and Th2 responses in wild-type and CD44-deficient mice in response to sheep RBC and chicken OVA, as well as examined Th1-Th2 differentiation in vivo and in vitro from CD44-sufficient and CD44-deficient naive CD4 T cells. We observed that deficiency of CD44 tended to inhibit Th1 while promoting Th2 differentiation. Furthermore, chimeric studies suggested that CD44 expression by CD4 T cells was essential for such Th2 bias. The regulation by CD44 occurred at the transcription level leading to up-regulated GATA3 and down-regulated T-bet expression in activated CD4 T cells. We also noted that CD44-deficiency could modify the state of dendritic cell subsets to induce a Th2-biased development. Results presented in this study demonstrate for the first time that CD44 participates in the regulation of Th1-Th2 differentiation. The Journal of Immunology, 2009, 183: 172-180.
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