期刊
CURRENT ALLERGY AND ASTHMA REPORTS
卷 12, 期 5, 页码 380-387出版社
CURRENT MEDICINE GROUP
DOI: 10.1007/s11882-012-0278-z
关键词
Respiratory syncytial virus (RSV); T cells; Epithelial cells; Nuclear factor-kappa B; NF-kappa B; Inflammation; Modulation; Airway; Immune; Response; Asthma; Bronchiolitis
资金
- National Institutes of Health [R01 HL 090664, R01 AI 070672, R01 AI 059108, GM 015431, R21 HL106446, U19AI095227]
- Veteran Affairs grant [1I01BX000624]
Respiratory syncytial virus (RSV) most often causes severe respiratory disease in the very young and the elderly. Acute disease can also cause exacerbations of asthma in any age group. Recent findings provide insight into how the innate and adaptive immune systems respond to RSV infection and provide preliminary evidence that these effects vary significantly by RSV strain and host. Components of cell signaling pathways that induce inflammatory cytokine expression during the innate immune response and alter epithelial cell polarity through activating transcription factors, namely NF-kappa B, are now more clearly understood. New studies also reveal how RSV infection skews T helper (Th) cell differentiation away from the cell-mediated Th1 subset and towards the Th2 subset. There are also new data supporting preferential Th17 differentiation during RSV infection. In addition, effective immune system regulation of IL-10 expression and T regulatory cell (Treg) airway accumulation are essential for effective RSV clearance.
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