Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: C3a is required for ILC2 function in allergic airway inflammation.

Authors: Gour, Naina; Smole, Ursula; Yong, Hwan-Mee; Lewkowich, Ian P; Yao, Nu; Singh, Anju; Gabrielson, Edward; Wills-Karp, Marsha; Lajoie, Stephane

Published In Mucosal Immunol, (2018 Nov)

Abstract: Aberrant type 2 responses underlie the pathologies in allergic diseases like asthma, yet, our understanding of the mechanisms that drive them remains limited. Recent evidence suggests that dysregulated innate immune factors can perpetuate asthma pathogenesis. In susceptible individuals, allergen exposure triggers the activation of complement, a major arm of innate immunity, leading to the aberrant generation of the C3a anaphylatoxin. C3 and C3a have been shown to be important for the development of Th2 responses, yet remarkably, the mechanisms by which C3a regulates type 2 immunity are relatively unknown. We demonstrate a central role for C3a in driving type 2 innate lymphoid cells (ILC2)-mediated inflammation in response to allergen and IL-33. Our data suggests that ILC2 recruitment is C3a-dependent. Further, we show that ILC2s directly respond to C3a, promoting type 2 responses by specifically: (1) inducing IL-13 and granulocyte-macrophage colony-stimulating factor, whereas inhibiting IL-10 production from ILC2; and (2) enhancing their antigen-presenting capability during ILC-T-cell cross-talk. In summary, we identify a novel mechanism by which C3a can mediate aberrant type 2 responses to aeroallergen exposure, which involves a yet unrecognized cross-talk between two major innate immune components-complement and group 2 innate lymphoid cells.

PubMed ID: 30104625 Exiting the NIEHS site

MeSH Terms: Allergens/immunology; Animals; Antigen Presentation; Asthma/immunology*; Cell Communication; Cell Movement; Cells, Cultured; Complement C3a/metabolism*; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism; Hypersensitivity/immunology*; Immunity, Innate; Inflammation/immunology*; Interleukin-10/metabolism; Interleukin-13/metabolism; Interleukin-33/immunology; Lymphocytes/immunology*; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Respiratory System/immunology*; Th2 Cells/immunology*

Back
to Top