SHP-1 regulates STAT6 phosphorylation and IL-4-mediated function in a cell type-specific manner

Zan Huang, John M. Coleman, Yan Su, Meredith Mann, John Ryan, Leonard D. Shultz, Hua Huang

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

SHP-1 has been shown to play positive and negative regulatory roles in IL-4-induced STAT6 phosphorylation and in IL-4-mediated functions. To determine whether SHP-1 can regulate STAT6 phosphorylation and IL-4-mediated functions in a cell type-specific manner in the immune system, we examined the IL-4 receptor (IL-4R) expression, STAT6 phosphorylation, and IL-4-mediated functions in CD4 + and CD8 + T cells of viable motheaten (me v/me v) and littermate control (+/-) mice. CD4 + T cells as well as CD8 + T cells from the lymph node of me v/me v and +/- mice expressed comparable levels of IL-4R. In CD4 + T cells, the loss of SHP-1 activity did not affect IL-4-induced STAT6 phosphorylation or IL-4-mediated function. In contrast, SHP-1-deficient CD8 + T cells from me v/me v mice failed to develop into IL-4-producing type-2 cytotoxic T cells (Tc2) in the presence of IL-4 despite that they showed comparable levels of STAT6 phosphorylation to that of +/- CD8 + T cells. Loss of SHP-1 activity also abolished IL-4-mediated inhibition of c-kit expression in bone marrow-derived mast cell (BMMC). Thus, our data suggest that SHP-1 may regulate IL-4-induced STAT6 phosphorylation and IL-4-mediated functions in a cell type-specific manner.

Original languageEnglish (US)
Pages (from-to)118-124
Number of pages7
JournalCytokine
Volume29
Issue number3
DOIs
StatePublished - Feb 7 2005

Keywords

  • IL-4 receptor expression
  • Signaling
  • Viable motheaten

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology

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