CD8+ T cells in asthma: Friend or foe?

被引:42
作者
Betts, Richard J.
Kemeny, D. Michael [1 ]
机构
[1] Natl Univ Singapore, Program Immunol, Ctr Life Sci, Singapore 119074, Singapore
关键词
Allergy; Asthma; T lymphocyte; CD8 T cell; CD4 T cell; IgE; ALLERGIC AIRWAY RESPONSES; BROWN-NORWAY RATS; HOMOCYTOTROPIC ANTIBODY FORMATION; OBSTRUCTIVE PULMONARY-DISEASE; SYNCYTIAL VIRUS-INFECTION; SOLUBLE-PROTEIN ANTIGENS; PERIPHERAL-BLOOD CD4(+); INHIBIT IGE RESPONSES; GAMMA-DELTA RECEPTOR; INTERFERON-GAMMA;
D O I
10.1016/j.pharmthera.2008.09.001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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. (c) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:123 / 131
页数:9
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