In vivo studies fail to reveal a role for IL-4 or STAT6 signaling in Th2 lymphocyte differentiation

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 I...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2008-08, Vol.105 (34), p.12423-12428
Main Authors: van Panhuys, Nicholas, Tang, Shiau-Choot, Prout, Melanie, Camberis, Mali, Scarlett, Debbie, Roberts, Joanna, Hu-Li, Jane, Paul, William E, Le Gros, Graham
Format: Article
Language:English
Subjects:
Allergens - immunology
Allergies
Animals
B lymphocytes
Biological Sciences
Cell Differentiation
Cells
Cytokines
Cytometry
Gene loci
Immunity
Infections
Interleukin-4 - physiology
Lymph nodes
Lymphocytes
Mice
Mice, Mutant Strains
Nippostrongylus - immunology
Parasites
Parasites - immunology
Rodents
Signal Transduction
STAT6 Transcription Factor - physiology
T lymphocytes
Th2 Cells - cytology
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Summary: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 during Nippostrongylus 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 that in 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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0806372105