The female genital tract possesses various systems of defenses against the infectious risk, which appear complementary, additive and even synergistic. These defenses comprise first non immune strategies, passive (synthesis of protective mucus; pH; epithelial barrier) or active (inflammatory reaction; secretion of humoral soluble factors such as lactoferrin), which are likely very efficient to limit the infectious inoculum. Pre-immune defense strategies, both humoral and cellular, yet not well understood, are also possibly involved in rapid protection pre-existing before antigenic stimulation. When these initial lines of defenses have failed, a third strategy, acquired and specific of the pathogen, occurs progressively. This latter associates humoral immune response, with secretory IgA (S-IgA) and IgM (S-IgM), and locally produced IgG (s-IgG), and cellular immune response. The very high amount of IgG in the female genital secretions, at levels more than 10-fold those of IgA, and originating in part from plasma by transudation, is remarkable for a corporeal fluid, the mucosal secretions being most often characterized by the predominance of immunoglobulins of the IgA isotype. The defenses of the female genital tract are largely under the influence of female hormones (menstrual cycle or pregnancy) and of paracrine production of various cytokines. Note that the genital defenses against infectious agents must not decrease the efficiency of the reproduction; indeed, spermatozoa act as potential exo-antigens for the female genital tract, and the inductive capabilities of the genital immunocompetent tissue have to be limited when the epithelial barrier has not been crossed. Systemic immunity acts in a second step to reinforce or substitute the acquired mucosal immunity of the genital tract.