期刊
JOURNAL OF VIROLOGY
卷 77, 期 8, 页码 4588-4596出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.77.8.4588-4596.2003
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资金
- NIAID NIH HHS [R01 AI049309, R01 AI051405, AI 49309, R01 AI034998, AI 34998, R21 AI034998] Funding Source: Medline
- NIGMS NIH HHS [GM 63244, T32 GM 072 15] Funding Source: Medline
Human cytomegalovirus (CMV) is a ubiquitous opportunistic pathogen that causes significant morbidity and mortality in immuncompromised people. An understanding of how CMV induces and circumvents host immunity is of critical importance in efforts to design effective therapeutics. It was recently discovered that mere cell contact by CMV particles leads to profound modulation of cellular gene expression, including induction of inflammatory cytokines and interferon-stimulated genes characteristic of innate immune detection. These findings suggest that a membrane receptor recognizes a CMV envelope protein(s), leading to innate immune activation. Here, we show that the pattern recognition receptors Toll-like receptor 2 (TLR2) and CD14 recognize CMV virions and trigger inflammatory cytokine production. Induction of inflammatory cytokines is mediated via TLR2-dependent activation of NF-kappaB. Since many of the pathological processes associated with CMV disease are facilitated or directly mediated by inflammatory cytokines, identification of the host membrane detection machinery may ultimately lead to improved therapeutics.
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