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Curr Allergy Asthma Rep. 2006 Feb;6(1):32-9.

Suppressor of cytokine signaling 3 (SOCS3) in Th2 cells evokes Th2 cytokines, IgE, and eosinophilia.

Author information

1
Laboratory for Signal Network, RIKEN Research Center for Allergy and Immunology (RCAI), RIKEN Yokohama Institute, Suehiro-cho 1-7-22, Tsurumi, Yokohama, Kanagawa 230-0045, Japan. raysolfc@rcai.riken.jp

Abstract

Atopic dermatitis, allergic rhinitis, and bronchial asthma are allergic immune disorders characterized by a predominance of T helper 2 (Th2) cells, the resulting elevation of allergen-specific immunoglobulin E (IgE), and mast cell- and eosinophil-associated inflammation. The cytokine environment at the site of the initial antigen stimulation determines the direction of helper T-cell differentiation into Th1 or Th2 cells. Therefore, negative regulators of cytokine signaling, suppressors of cytokine signaling (SOCS) proteins, play an important role in Th2-mediated allergic responses through the control of the balance between Th1 and Th2 cells. SOCS3 and SOCS5 are predominantly expressed in Th2 and Th1 cells, respectively, and they reciprocally inhibit the Th1 and Th2 differentiation processes. In this article, we discuss the role of SOCS3 and SOCS5 proteins in atopic asthma and allergic conjunctivitis and explore the potential of SOCS proteins as targets for therapeutic strategies in allergic disorders.

PMID:
16476192
[Indexed for MEDLINE]

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