CD43 regulates Th2 differentiation and inflammation

Judy L. Cannon, Amélie Collins, Purvi D. Mody, Diwaker Balachandran, Kammi J. Henriksen, Cassandra E. Smith, Jiankun Tong, Bryan S. Clay, Stephen D. Miller, Anne I. Sperling

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

CD43 is a highly glycosylated transmembrane protein that regulates T cell activation. CD43-/- T cells are hyperproliferative and the cytoplasmic tail of CD43 has been found to be sufficient to reconstitute wild-type proliferation levels, suggesting an intracellular mechanism. In this study, we report that upon TCR ligation CD43-/- T cells demonstrated no increase in tyrosine phosphorylation but a decreased calcium flux. Interestingly, CD43-/- T cells preferentially differentiated into Th2 cells in vitro, and CD43-/- T cells show increased GATA-3 translocation into the nucleus. In vivo, CD43-/- mice exhibited increased inflammation in two separate models of Th2-mcdiated allergic airway disease. In contrast, in Th1-mediated diabetes, nono-bese diabetic CD43 -/- mice did not significantly differ from wild-type mice in disease onset or progression. Th1-induced experimental autoimmune encephalomyelitis to M0G35-55 was also normal in the CD43-/- mice. Nonetheless, the CD43-/-mice produced more IL-5 when restimulated with MOG 35-55 in vitro and demonstrated decreased delayed-type hypersensitivity responses. Together, these data demonstrate that although CD43-/- T cells preferentially differentiate into Th2 cells, this response is not sufficient to protect against Thl-mediated autoimmune responses.

Original languageEnglish (US)
Pages (from-to)7385-7393
Number of pages9
JournalJournal of Immunology
Volume180
Issue number11
DOIs
StatePublished - 2008

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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