» Articles » PMID: 22561831

Innate and Adaptive Immune Responses in Asthma

Overview
Journal Nat Med
Date 2012 May 8
PMID 22561831
Citations 367
Authors
Affiliations
Soon will be listed here.
Abstract

The recognition that asthma is primarily an inflammatory disorder of the airways associated with T helper type 2 (T(H)2) cell-dependent promotion of IgE production and recruitment of mast cells and eosinophils has provided the rationale for disease control using inhaled corticosteroids and other anti-inflammatory drugs. As more has been discovered about the cytokine, chemokine and inflammatory pathways that are associated with T(H)2-driven adaptive immunity, attempts have been made to selectively inhibit these in the hope of discovering new therapeutics as predicted from animal models of allergic inflammation. The limited success of this approach, together with the recognition that asthma is more than allergic inflammation, has drawn attention to the innate immune response in this disease. Recent advances in our understanding of the sentinel role played by innate immunity provides new targets for disease prevention and treatment. These include pathways of innate stimulation by environmental or endogenous pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) to influence the activation and trafficking of DCs, innate sources of cytokines, and the identification of new T cell subsets and lymphoid cells.

Citing Articles

Social vulnerability and asthma-related emergency medical services in Illinois.

Geiger S, Khaium M, Gustafson E, Shapiro M, Keeley S, Johnson C Front Public Health. 2025; 13:1521545.

PMID: 40078769 PMC: 11897263. DOI: 10.3389/fpubh.2025.1521545.


An Updated Review on the Use of Noninvasive Respiratory Supports in the Management of Severe Asthma Exacerbations.

Cuttone G, La Via L, Pappalardo F, Sorbello M, Paterno D, Piattoli M Medicina (Kaunas). 2025; 61(2).

PMID: 40005443 PMC: 11857382. DOI: 10.3390/medicina61020328.


Incidence and risk factors of serious infections occurred in patients with lung cancer following immune checkpoint blockade therapy.

Wang X, Wu Y, Hu W, Zhang J BMC Cancer. 2025; 25(1):307.

PMID: 39979857 PMC: 11843754. DOI: 10.1186/s12885-025-13743-7.


Repeated and alternate stimulations with dsRNA and SEB alter responses in macrophages and epithelial cells.

Choi J, Kim Y, Kim M, Kang M, Hwang Y, Yoon J World Allergy Organ J. 2025; 18(2):101026.

PMID: 39925983 PMC: 11804812. DOI: 10.1016/j.waojou.2025.101026.


IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential.

Sheng F, Li M, Yu J, Yang S, Zou L, Yang G Front Immunol. 2025; 16:1533335.

PMID: 39925809 PMC: 11802536. DOI: 10.3389/fimmu.2025.1533335.


References
1.
van Panhuys N, Prout M, Forbes E, Min B, Paul W, Le Gros G . Basophils are the major producers of IL-4 during primary helminth infection. J Immunol. 2011; 186(5):2719-28. PMC: 3488853. DOI: 10.4049/jimmunol.1000940. View

2.
Busse W, Israel E, Nelson H, Baker J, Charous B, Young D . Daclizumab improves asthma control in patients with moderate to severe persistent asthma: a randomized, controlled trial. Am J Respir Crit Care Med. 2008; 178(10):1002-8. DOI: 10.1164/rccm.200708-1200OC. View

3.
Hilty M, Burke C, Pedro H, Cardenas P, Bush A, Bossley C . Disordered microbial communities in asthmatic airways. PLoS One. 2010; 5(1):e8578. PMC: 2798952. DOI: 10.1371/journal.pone.0008578. View

4.
Veldhoen M, Uyttenhove C, Van Snick J, Helmby H, Westendorf A, Buer J . Transforming growth factor-beta 'reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset. Nat Immunol. 2008; 9(12):1341-6. DOI: 10.1038/ni.1659. View

5.
Kon O, Sihra B, Loh L, Barkans J, Compton C, Barnes N . The effects of an anti-CD4 monoclonal antibody, keliximab, on peripheral blood CD4+ T-cells in asthma. Eur Respir J. 2001; 18(1):45-52. DOI: 10.1183/09031936.01.00064101. View