Pathogenic mechanisms of P-aeruginosa keratitis:: A review of the role of T cells, Langerhans cells, PMN, and cytokines
Pathogenic mechanisms of P-aeruginosa keratitis:: A review of the role of T cells, Langerhans cells, PMN, and cytokines
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DOI：
10.1089/10445490260099665
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发表时间：
2002-05-01
影响因子：
3.1
通讯作者：
Hazlett, LD
中科院分区：
文献类型：
--
作者：
Hazlett, LD
本文的目的是回顾我们目前的理解的作用，细胞因子，趋化因子，T细胞，朗格汉斯细胞，中性粒细胞（PMN）和它们的相互作用在体内的宿主响应铜绿假单胞菌眼部挑战。体内的细胞/细胞因子网络已经开始被解开，讨论的数据提供了实质性的证据，CD 4（+）T细胞（Th 1型）的调节作用，直接有助于在敏感的C57 BL/6（角膜穿孔）与耐药的BALB/c（角膜愈合）小鼠的角膜PMN的持久性。此外，在易感小鼠模型中，CD 4 + T细胞与朗格汉斯细胞相互作用，B7/CD 28连接似乎对抗原呈递和易感性应答至关重要。各种细胞因子和趋化因子（例如，MIP-1 α、IL-1 β、MIP-2、IL-12和IFN-γ）及其在易感小鼠与耐药小鼠中感染后持续上调的模式也将根据体内细胞因子网络进行讨论。T细胞介导的致病机制在对铜绿假单胞菌眼部感染的易感性反应的发展中具有重要意义。在没有T细胞浸润到角膜中的情况下，PMN不会持续存在于基质中，并且细胞因子和趋化因子更好地平衡，导致基质破坏和抵抗反应减少。
The aim of this article is to review our current understanding of the role of cytokines, chemokines, T cells, Langerhans cells, and neutrophils (PMN) and their interactions in vivo in the host response to Pseudomonas aeruginosa ocular challenge. The cellular/cytokine network in vivo has begun to be unraveled, and the data discussed provide substantive evidence for a regulatory role of CD4(+) T cells (Th1 type) contributing directly to persistence of PMN in the cornea of susceptible C57BL/6 (cornea perforates) versus resistant BALB/c (cornea heals) mice. Additionally, in the susceptible mouse model, CD4+ T cells interact with Langerhans cells and B7/CD28 ligation appears critical for antigen presentation and the susceptibility response. Various cytokines and chemokines (e.g., MIP-1alpha, IL-1beta, MIP-2, IL-12, and IFN-gamma) and their pattern of sustained upregulation after infection in susceptible versus resistant mice also will be discussed in light of an in vivo cytokine network. T-cell-mediated pathogenic mechanisms are of importance in development of the susceptible response to P. aeruginosa ocular infection. In the absence of T-cell infiltration into the cornea, PMN do not persist in the stroma, and cytokines and chemokines are better balanced, resulting in decreased stromal destruction and the resistance response.