TGF-βresponsive myeloid cells suppress type 2 immunity and emphysematous pathology after hookworm infection

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Abstract

Transforming growth factor β (TGF-β) regulates inflammation, immunosuppression, and wound-healing cascades, but it remains unclear whether any of these functions involve regulation of myeloid cell function. The present study demonstrates that selective deletion of TGF-βRII expression in myeloid phagocytes i) impairs macrophage-mediated suppressor activity, ii) increases baseline mRNA expression of proinflammatory chemokines/cytokines in the lung, and iii) enhances type 2 immunity against the hookworm parasite Nippostrongylus brasiliensis. Strikingly, TGF-βresponsive myeloid cells promote repair of hookworm-damaged lung tissue, because LysMCreTGF- βRIIflox/floxmice develop emphysema more rapidly than wild-type littermate controls. Emphysematous pathology in LysMCreTGF- βRIIflox/floxmice is characterized by excessive matrix metalloprotease (MMP) activity, reduced lung elasticity, increased total lung capacity, and dysregulated respiration. Thus, TGF-β effects on myeloid cells suppress helminth immunity as a consequence of restoring lung function after infection. © 2012 American Society for Investigative Pathology.

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APA

Heitmann, L., Rani, R., Dawson, L., Perkins, C., Yang, Y., Downey, J., … Herbert, D. R. (2012). TGF-βresponsive myeloid cells suppress type 2 immunity and emphysematous pathology after hookworm infection. American Journal of Pathology, 181(3), 897–906. https://doi.org/10.1016/j.ajpath.2012.05.032

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