Chlamydial interferon gamma immune evasion influences infection tropism.
Chlamydial interferon gamma immune evasion influences infection tropism.
复制标题
衣原体干扰素γ免疫逃避影响感染趋向性。
DOI：
10.1016/j.mib.2006.12.003
复制
发表时间：
2007
影响因子：
5.4
通讯作者：
Nelson,DavidE
中科院分区：
文献类型：
--
作者：
McClarty,Grant;Caldwell,HarlanD;Nelson,DavidE
Chlamydia trachomatis is a human pathogen and Chlamydia muridarum is a mouse pathogen but paradoxically, they share near genomic synteny. The majority of strain-variable genes are located primarily in a hyper-variable region termed the plasticity zone. Tryptophan synthase and cytotoxin are plasticity zone genes unique to the human and murine strains, respectively. Tryptophan synthase is a virulence factor that differentiates C. trachomatis strains into genital and ocular disease pathotypes, whereas cytotoxin(s) is a virulence factor linked to murine infection tropism. Divergence in these loci is strongly correlated with host-specific interferon gamma effector activities, suggesting that these virulence genes have co-evolved with their respective hosts as a primary mechanism to evade innate immunity. These findings have important implications for chlamydial animal modeling studies.
