**6. B cells and antibodies**

B cells support the immune response in a variety of ways. Effector mechanisms such as antibody-mediated neutralization and opsonization [117], antibody-dependent cellular cytotoxicity (ADCC) [118], induction of phagocytosis, and antigen presentation to CD4 T cells by binding of antigen-antibody complexes to Fc receptors in APC [102] have been identified.

The role of B cells in the immune response against Chlamydia has been the subject of many studies. It is known that many *C. trachomatis* proteins, including the major outer membrane protein, induce the formation of specific antibodies [119]. It has also been shown *in vitro* that anti-chlamydial antibodies are neutralizing [71, 117]. However, there is evidence to suggest that B cells play

#### *Immune Response to Chlamydia DOI: http://dx.doi.org/10.5772/intechopen.110799*

an important role in the secondary memory response rather than the primary infection. It was determined that primary genital infection with *C. muridarum* in mice lacking B cells did not show a different course than in wild-type mice [120], while mice with B cell deficit were more susceptible to reinfection [121]. Mice that cleared primary genital tract infection were found to be resistant to reinfection even after experimental depletion of CD4 and CD8 T cells. It was observed that B cell-deficient mice were unable to resolve the secondary infection after CD4 T cell depletion [122]. It has been reported that passive immune serum transfer to naïve mice does not provide protection, but CD4 T cells prepared from antigen-experienced mice and immune serum together provide optimum protection [123]. The protective effects of the antibodies are likely due to their ability to activate Th1 cells and enhance cellular immune responses [124]. The detection of high antibody titers associated with infertility rather than infection control in epidemiological studies indicates that the humoral response may also have negative effects [125]. However, data on pathogenic antibodies are limited. One of the antibodies discussed in relation to its contribution to pathology is anti-HSP antibodies. HSPs are a group of chaperones, proteins that ensure the correct folding of intracellular proteins: They are found in both eukaryotic and prokaryotic organisms. Its levels increase when cells are exposed to temperature rises, oxidative stress, and inflammation. HSPs, mainly HSP60, are produced by *C. trachomatis* during infection. HSP60 has high immunogenicity. It is quite similar to human HSP60. Therefore, it is suggested that it may trigger an autoimmune response that leads to pathology. High antibody titers against HSP60 were found to be associated with pelvic inflammatory disease, ectopic pregnancy, and trachoma scar [126].

The effects elicited by the response to HSP60 during *C. trachomatis* infection are thought to be similar in *C. pneumonia* infection. It has been suggested that HSP60 released from infected epithelium and macrophages during recurrent and persistent infection with *C. pneumonia* produces immunopathological results [127].

Antibodies against *C. pneumonia* are also used in seroepidemiological studies investigating the relationship between *C. pneumoniae* infection and inflammatory diseases. It has been suggested that IgA levels are a better marker than IgG, especially in terms of detecting chronic infection [128].

*Chlamydia – Secret Enemy from Past to Present*
