T. pallidum infection evokes cellular and humoral immune responses. The humoral response manifested by production of phospholipid and treponemal antibodies is the basis for serodiagnosis of syphilis. The phospholipid or cardiolipin antibodies are detected by a variety of flocculation tests using a defined mixture of cardiolipin-lecithin-cholesterol as antigen (Venereal Disease Research Laboratory, VDRL antigen or VDRL test). A second type of antibody, known as cardiolipin F (detected by immunofluorescence) and directed against host-cell mitochondrial cardiolipin (autoantibody), is also associated with syphilis, but is not used for serodiagnosis. Treponemal antibodies, once detected by the cumbersome T. pallidum immobilization test (TPI) are now identified by immunofluorescence (FTA-ABS) or microhemagglutination test (MHA-TP). Treponemal antibodies appear after infection almost simultaneously with the cardiolipin antibodies. The treponemal antibodies persist in the host for many years even after treatment, whereas the cardiolipin antibodies parallel the dynamics of the infection and are useful in interpreting the efficacy of treatment. Autoantibodies to tissue phospholipids and other tissue constituents, to blood cells and serum globulins are also produced by T. pallidum-infected hosts.
Cell-mediated immune responses to infectious organisms involve activation of macrophages and the induction of CD8 T cells and helper CD4 T cells. The various subsets of CD4 T cells, and the cytokines they produce, play a crucial role in determining the outcome of infectious disease in terms of both protective immunity and immunopathology. Although a switch from T helper TH1 to TH2 immune response has been observed in the rabbit experimental model of syphilis, this remains to be further studied.
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