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Host responses in syphilis and gonorrhea. (a) A dominant Th1 response in primary syphilis promotes IFN-γ production. Opsonized treponemas in secondary syphilis undergo phagocytosis and resistant treponemas disseminate and produce skin and mucosal lesions. (b) Neisseria gonorrhoeae inhibits complement pathways and Th1 and Th2 cells but stimulates Th17 cells which promote neutrophil infiltration. Some gonococci may escape phagocytosis and invade pelvic organs.
