Skip to main page content
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.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Oct 25;21(11):45.
doi: 10.1007/s11882-021-01022-x.

The Role of PPAR-γ in Allergic Disease

Affiliations
Review

The Role of PPAR-γ in Allergic Disease

Julian M Stark et al. Curr Allergy Asthma Rep. .

Abstract

Purpose of review: The incidence of allergic diseases such as asthma, rhinitis and atopic dermatitis has risen at an alarming rate over the last century. Thus, there is a clear need to understand the critical factors that drive such pathologic immune responses. Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor that has emerged as an important regulator of multiple cell types involved in the inflammatory response to allergens; from airway epithelial cells to T Helper (TH) cells.

Recent findings: Initial studies suggested that agonists of PPAR-γ could be employed to temper allergic inflammation, suppressing pro-inflammatory gene expression programs in epithelial cells. Several lines of work now suggest that PPAR-γ plays an essential in promoting 'type 2' immune responses that are typically associated with allergic disease. PPAR-γ has been found to promote the functions of TH2 cells, type 2 innate lymphoid cells, M2 macrophages and dendritic cells, regulating lipid metabolism and directly inducing effector gene expression. Moreover, preclinical models of allergy in gene-targeted mice have increasingly implicated PPAR-γ in driving allergic inflammation. Herein, we highlight the contrasting roles of PPAR-γ in allergic inflammation and hypothesize that the availability of environmental ligands for PPAR-γ may be at the heart of the rise in allergic diseases worldwide.

Keywords: Allergy; Asthma; ILC2; Lipid metabolism; PPAR-γ; TH2.

PubMed Disclaimer

Conflict of interest statement

The authors declare no competing interests.

Similar articles

Cited by

References

    1. Akdis CA, Agache I. Global atlas of allergy. European Academy of Allergy and Clinical Immunology. 2014.
    1. Lambrecht BN, Hammad H. The immunology of asthma, Nat Immunol, Research Support, Non-U.S. Gov't. 2015;16(1):45–56. 10.1038/ni.3049. - PubMed
    1. Abrahamsson TR, Wu RY, Jenmalm MC. Gut microbiota and allergy: the importance of the pregnancy period. Pediatr Res. 2015;77(1):214–219. doi: 10.1038/pr.2014.165. - DOI - PubMed
    1. Asher MI, et al. Which population level environmental factors are associated with asthma, rhinoconjunctivitis and eczema? Review of the ecological analyses of ISAAC Phase One, Respiratory research. 2010;11(1):1–10. - PMC - PubMed
    1. Issemann I, Green S. Activation of a member of the steroid hormone receptor superfamily by peroxisome proliferators. Nature. 1990;347(6294):645–650. doi: 10.1038/347645a0. - DOI - PubMed

Publication types