Open AccessIn vivo studies fail to reveal a role for IL-4 or STAT6 signaling in Th2 lymphocyte differentiation
Author(s) -
Nicholas J. Van Panhuys,
Shiau Choot Tang,
Melanie Prout,
Mali Camberis,
Debbie Scarlett,
Joanna M. Roberts,
Jane HuLi,
William E. Paul,
Graham Le Gros
Publication year - 2008
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.0806372105
Subject(s) - stat6 , interleukin 4 , biology , immune system , nippostrongylus brasiliensis , immunology , microbiology and biotechnology , cellular differentiation , interleukin 13 , immunity , in vivo , effector , gene , genetics
The expression of interleukin-4 (IL-4) is viewed as the hallmark of a Th2 lymphocyte, whereas the subsequent action of IL-4 and IL-13, mediated through the STAT6 signaling pathway, is seen as a prerequisite for the full development of Th2 immune responses to parasites and allergens. G4 mice, whose IL-4 gene locus contains the fluorescent reporter eGFP, were used to quantify the number of Th2 cells that develop duringNippostrongylus brasiliensis - or allergen-induced immune responses under conditions where IL-4 or STAT6 was absent. Here, we show that deletion of IL-4 or STAT6 had little impact on the number or timing of appearance of IL-4-producing Th2 cells. These data indicate thatin vivo differentiation of naïve CD4 T cells to Th2 status often occurs independently of IL-4 and STAT6 and that recently described pathways of Th2 cell differentiation may explain how allergens and parasites selectively induce Th2-mediated immunity.