Ram S, Mackinnon F G, Gulati S, McQuillen D P, Vogel U, Frosch M, Elkins C, Guttormsen H K, Wetzler L M, Oppermann M, Pangburn M K, Rice P A
The Maxwell Finland Laboratory for Infectious Diseases, Boston Medical Center, MA 02118, USA.
Mol Immunol. 1999 Sep-Oct;36(13-14):915-28. doi: 10.1016/s0161-5890(99)00114-5.
Neisseria gonorrhoeae and Neisseria meningitidis have evolved intricate mechanisms to evade complement-mediated killing. Sialylation of gonococcal lipooligosaccharide (LOS) results in conversion of previously serum sensitive strains to unstable serum resistance, which is mediated by factor H binding. Porin (Por) is also instrumental in mediating stable serum resistance in gonococci. The 5th loop of certain gonococcal PorlAs binds factor H, which efficiently inactivates C3b to iC3b. Factor H glycan residues may be essential for factor H binding to certain Por1A strains. Por1A strains can also regulate the classical pathway by binding to C4b-binding protein (C4bp) probably via the 1st loop of the Por molecule. Certain serum resistant Por1 B strains can also regulate complement by binding C4bp through a loop other than loop 1. Purified C4b can inhibit binding of C4bp to Por 1B, but not Por1A, suggesting different binding sites on C4bp for the two Por types. Unlike serum resistant gonococci, resistant meningococci have abundant C3b on their surface, which is only partially processed to iC3b. The main mechanism of complement evasion by group B meningococci is inhibition of membrane attack complex (MAC) insertion by their polysaccharide capsule. LOS structure may act in concert with capsule to prevent MAC insertion. Meningococcal strains with Class 3 Por preferentially bind factor H, suggesting Class 3 Por acts as a receptor for factor H.
淋病奈瑟菌和脑膜炎奈瑟菌已经进化出复杂的机制来逃避补体介导的杀伤作用。淋球菌脂寡糖（LOS）的唾液酸化导致先前血清敏感菌株转变为不稳定的血清抗性，这是由因子H结合介导的。孔蛋白（Por）在介导淋球菌的稳定血清抗性方面也起作用。某些淋球菌Por1A的第5环结合因子H，其可有效地将C3b灭活为iC3b。因子H聚糖残基对于因子H与某些Por1A菌株的结合可能至关重要。Por1A菌株还可能通过Por分子的第1环与C4b结合蛋白（C4bp）结合来调节经典途径。某些血清抗性Por1B菌株也可以通过除第1环以外的环结合C4bp来调节补体。纯化的C4b可以抑制C4bp与Por1B的结合，但不能抑制与Por1A的结合，这表明C4bp上两种Por类型的结合位点不同。与血清抗性淋球菌不同，抗性脑膜炎球菌表面有丰富的C3b，其仅部分加工为iC3b。B群脑膜炎球菌逃避补体的主要机制是通过其多糖荚膜抑制膜攻击复合物（MAC）插入。LOS结构可能与荚膜协同作用以防止MAC插入。具有3类Por的脑膜炎球菌菌株优先结合因子H，表明3类Por作为因子H的受体。
