STAT3 is a central regulator of lymphocyte differentiation and function

Alisa Kane, Elissa K. Deenick, Cindy S. Ma, Matthew C. Cook, Gulbu Uzel, Stuart G. Tangye*

*Corresponding author for this work

    Research output: Contribution to journalReview articlepeer-review

    76 Citations (Scopus)

    Abstract

    Signalling in lymphocytes through cytokine receptors is critical for their development, activation and differentiation into effector cells that mediate protection against pathogens and provide the host with protective immunological memory. The essential role of cytokine signalling has been established not only by the generation and examination of gene-targeted mice, but also 'Experiments of Nature' whereby monogenic mutations cause primary immunodeficient conditions characterised by impaired immunity to infectious diseases due to compromised lymphocyte function. Mutations in STAT3 cause autosomal dominant hyper-IgE syndrome. Here, we will review how the study of STAT3-deficient individuals has revealed non-redundant functions of STAT3 and specific cytokines in human lymphocyte biology, and have delineated mechanisms underlying the distinct clinical features of autosomal dominant hyper-IgE syndrome.

    Original languageEnglish
    Pages (from-to)49-57
    Number of pages9
    JournalCurrent Opinion in Immunology
    Volume28
    Issue number1
    DOIs
    Publication statusPublished - Jun 2014

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