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JAKSTAT. 2013 Oct 1;2(4):e25301. doi: 10.4161/jkst.25301. Epub 2013 Jun 10.

STAT6 and lung inflammation.

Author information

1
Department of Medicine; University of California, San Diego; La Jolla, CA USA ; Department of Pediatrics; University of California, San Diego; La Jolla, CA USA.
2
Department of Medicine; University of California, San Diego; La Jolla, CA USA.

Abstract

Lung inflammation has many etiologies, including diseases of Th2-type immunity, such as asthma and anti-parasitic responses. Inflammatory diseases of the lung involve complex interactions among structural cells (airway epithelium, smooth muscle, and fibroblasts) and immune cells (B and T cells, macrophages, dendritic cells, and innate lymphoid cells). Signal transducer and activator of transcription 6 (STAT6) has been demonstrated to regulate many pathologic features of lung inflammatory responses in animal models including airway eosinophilia, epithelial mucus production, smooth muscle changes, Th2 cell differentiation, and IgE production from B cells. Cytokines IL-4 and IL-13 that are upstream of STAT6 are found elevated in human asthma and clinical trials are underway to therapeutically target the IL-4/IL-13/STAT6 pathway. Additionally, recent work suggests that STAT6 may also regulate lung anti-viral responses and contribute to pulmonary fibrosis. This review will focus on the role of STAT6 in lung diseases and mechanisms by which STAT6 controls immune and structural lung cell function.

KEYWORDS:

IL-13; IL-4; STAT6; Th2; asthma

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