Authors: Tamas Fulop; Anis Larbi¹; Nadine Douziech¹; Carl Fortin¹; Kal-Philippe Guérard¹; Olivier Lesur²; Abdelouahed Khalil¹; Gilles Dupuis³

Source: Aging Cell, Volume 3, Number 4, August 2004 , pp. 217-226(10)

Publisher: Wiley-Blackwell

Abstract:

Summary

It is well known that the immune response decreases during aging, leading to a higher susceptibility to infections, cancers and autoimmune disorders. Most widely studied have been alterations in the adaptive immune response. Recently, the role of the innate immune response as a first-line defence against bacterial invasion and as a modulator of the adaptive immune response has become more widely recognized. One of the most important cell components of the innate response is neutrophils and it is therefore important to elucidate their function during aging. With aging there is an alteration of the receptor-driven functions of human neutrophils, such as superoxide anion production, chemotaxis and apoptosis. One of the alterations underlying these functional changes is a decrease in signalling elicited by specific receptors. Alterations were also found in the neutrophil membrane lipid rafts. These alterations in neutrophil functions and signal transduction that occur during aging might contribute to the significant increase in infections in old age.

Keywords: aging; apoptosis; chemotaxis; free radicals; lipid rafts; neutrophils; signal transduction; TLRs

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1474-9728.2004.00110.x

Affiliations: 1: Centre de Recherche sur le Vieillissement, Programme d’Immunologie 2: Service de Pneumologie 3: Département de Biochimie, Département de Médecine, Université de Sherbrooke, Sherbrooke, Québec, Canada

Publication date: 2004-08-01

Related content

• In this: publication
• By this: publisher
• In this Subject: Genetics
• By this author: Tamas Fulop ;  Anis Larbi ;  Nadine Douziech ;  Carl Fortin ;  Kal-Philippe Guérard ;  Olivier Lesur ;  Abdelouahed Khalil ;  Gilles Dupuis

Website © Publishing Technology. Article copyright remains with the publisher, society or author(s) as specified within the article.

• Terms and conditions
• Privacy policy
• Information for advertisers