Back to Search Start Over

CD8+ T cells in asthma: friend or foe?

Authors :
Betts RJ
Kemeny DM
Source :
Pharmacology & therapeutics [Pharmacol Ther] 2009 Feb; Vol. 121 (2), pp. 123-31. Date of Electronic Publication: 2008 Oct 01.
Publication Year :
2009

Abstract

While it is well established that CD4(+) T lymphocytes play a crucial role in the initiation, progression and persistence of asthma, the role of CD8(+) T cells is less understood. CD8(+) T cells form functionally similar subsets which exhibit similar cytokine profiles as Th1 and Th2 cells, known as Tc1 and Tc2. Evidence from animal studies suggest that CD8(+) T cells are capable of regulating IgE production through the induction of IL-12 and IL-18 production in dendritic cells, and that CD8(+) T cells may act to moderate Th2 polarisation within the localised lymph nodes during allergic sensitisation. Such findings have led to the suggestion that Th1 polarising, CD8(+) T cell-inducing vaccines would inhibit the development of airway hyperresponsiveness (AHR) and Th2 cell infiltration. Despite these positive findings, the role of CD8(+) T cells within the lung remains poorly understood. While CD8(+) T cells, particularly those expressing the Tc1 phenotype, are capable of moderating inflammation and suppressing AHR, it has been postulated that Tc2 CD8(+) T cells predominate within established asthma and may act to amplify the inappropriate immune response which defines the condition. Within the clinic, the association between CD8(+) T cells and asthma is almost universally defined as injurious, further suggesting a prejudicial role for these cells within the established disease. CD8(+) T cells may be a valuable potential target for therapeutic intervention, either by potentiating their regulatory effects prior to the development of sensitisation, or through suppressing their pro-inflammatory properties within established atopy.

Details

Language :
English
ISSN :
0163-7258
Volume :
121
Issue :
2
Database :
MEDLINE
Journal :
Pharmacology & therapeutics
Publication Type :
Academic Journal
Accession number :
18940198
Full Text :
https://doi.org/10.1016/j.pharmthera.2008.09.001