International Immunology, Vol. 15, No. 6, pp. 701-710,
June 2003
© 2003 Japanese Society for Immunology
Differential regulation of VLA-2 expression on Th1 and Th2 cells: a novel marker for the classification of Th subsets
1 Division of Immunoregulation, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan
Correspondence to: T. Nishimura; E-mail: tak24{at}imm.hokudai.ac.jp
Transmitting editor: T. Saito
We found that Th1 cells derived from ovalbumin (OVA)-specific TCR transgenic (DO11.10) mice showed significantly higher levels of VLA-2 (CD49b/CD29) expression than Th2 cells. In the early days (until 6 days) during induction of Th1 or Th2 cells, the expression of VLA-2 was gradually increased on both Th subsets. Thereafter, VLA-2 expression was further up-regulated on Th1 cells until 13 days, while a significant decrease of VLA-2 was observed in Th2 cells, resulting in a marked difference of expression at day 13. Up-regulation of VLA-2 on Th1 cells was not impaired in IFN-
–/– Th cells nor blocked by anti-IL-12 mAb treatment on wild-type Th cells, suggesting that up-regulation of VLA-2 on Th1 cells occurs in an IFN-- and IL-12-independent manner. In contrast, Th cells cultured under IL-4-depleted Th2 conditions abrogated the down-regulation of VLA-2 expression, suggesting that down-regulation of VLA-2 expression on Th2 cells was dependent on IL-4. The finding that STAT6–/– Th2 cells did not show any down-regulation of VLA-2 expression and expressed the same levels of VLA-2 as Th1 cells indicated a critical role for the IL-4 receptor/STAT6 signaling pathway in IL-4-depedent down-regulation of VLA-2 on Th2 cells. Stimulation of Th1 cells by VLA-2 ligands such as collagen type I or agonistic mAb provided co-stimulation for anti-CD3 mAb-induced IFN- production. However, these ligations had little effect on the IL-4 production of Th2 cells. Together, these results indicate that VLA-2 is a novel functional marker that dissociates Th1 from Th2 cells, and thus might be useful for therapeutic monitoring of Th1-dependent immune diseases such as rheumatoid arthritis or Crohn’s disease.
Keywords: CD49b, CD29, integrin, IL-4, STAT6
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