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Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis.

Abstract：

:The roles of macrophages in type 2-driven inflammation and fibrosis remain unclear. Here, using CD11b-diphtheria toxin receptor (DTR) transgenic mice and three models of interleukin 13 (IL-13)-dependent inflammation, fibrosis, and immunity, we show that CD11b(+) F4/80(+) Ly6C(+) macrophages are required for the maintenance of type 2 immunity within affected tissues but not secondary lymphoid organs. Direct depletion of macrophages during the maintenance or resolution phases of secondary Schistosoma mansoni egg-induced granuloma formation caused a profound decrease in inflammation, fibrosis, and type 2 gene expression. Additional studies with CD11c-DTR and CD11b/CD11c-DTR double-transgenic mice suggested that macrophages but not dendritic cells were critical. Mechanistically, macrophage depletion impaired effector CD4(+) T helper type 2 (Th2) cell homing and activation within the inflamed lung. Depletion of CD11b(+) F4/80(+) Ly6C(+) macrophages similarly reduced house dust mite-induced allergic lung inflammation and suppressed IL-13-dependent immunity to the nematode parasite Nippostrongylus brasiliensis. Consequently, therapeutic strategies targeting macrophages offer a novel approach to ameliorate established type 2 inflammatory diseases.

journal_name

Mucosal Immunol

journal_title

Mucosal immunology

authors

Borthwick LA,Barron L,Hart KM,Vannella KM,Thompson RW,Oland S,Cheever A,Sciurba J,Ramalingam TR,Fisher AJ,Wynn TA

doi

10.1038/mi.2015.34

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

38-55

issue

1

eissn

1933-0219

issn

1935-3456

pii

mi201534

journal_volume

9

pub_type

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