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Curr Opin Pharmacol. 2009 Aug;9(4):454-61. doi: 10.1016/j.coph.2009.04.001. Epub 2009 May 19.

TGF-beta can leave you breathless.

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Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4352, United States.


Transforming growth factor-beta (TGF-beta), a ubiquitous and multifunctional cytokine, is central to the evolution and modulation of host defense. Early on, TGF-beta was recognized for its chemotactic and pro-inflammatory properties, but then identification of its powerful suppressive activities focused attention on dissecting its mechanisms of immune inhibition. Just as quickly as TGF-beta-mediated regulation of a population of CD4(+)CD25(+)Foxp3(+) regulatory T cells became the rage, a surprising finding that TGF-beta was the impetus behind a subset of pro-inflammatory T helper (Th)17 cells brought back a re-emphasis on its broader ability to dictate inflammatory events. Emerging evidence indicates that much remains to be discovered regarding the complex and intertwined roles of TGF-beta in inflammation, T cell lineage commitment, antibody generation, immune suppression, and tolerance. While it may appear that TGF-beta has multiple, ill-defined, contradictory and overlapping modes of activity that are impossible to unravel, the current excitement for dissecting how TGF-beta controls immunity defines a challenge worthy of pursuit. The lung is particularly vulnerable to the influences of TGF-beta, which is produced by its immune and non-immune cell populations. In its absence, lung pathology becomes lethal, whereas TGF-beta overproduction also has untoward consequences, potentially leaving one breathless, and underscoring the paradoxical, but essential contribution of TGF-beta to tissue and immune homeostasis.

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