**2.5 Dendritic cell**

The DCs, which are professional antigen presenting cells (APC), have been shown to activate both CD4 and CD8 T cells through MHC class I/II presentation in Chlamydial infections [63, 64]. In a murine model, DCs appear to harbor infectious *C. muridarum* but can still present antigen to T cells. TLR2, STING, and NLRs in DC lead to the production of proinflammatory cytokines such as IL-6, TNF-a, CCR7, CXCL10, IL-1a, and IL-12 after uptake of Chlamydia. These cytokines ensure DC maturation and optimal antigen presentation [65]. Cytokines produced by DC and process of processing and presenting antigens to T cells determine the Th1/Th2 balance of the adaptive response during chlamydial infection. Upon preferential antigen uptake, preferential production of IL-12 from DC occurs. IL-12 activates naive CD4 T lymphocytes and enables them to differentiate toward the Th1 subgroup [66]. In a study, when DCs stimulated with recombinant chlamydial proteins were adoptively transferred to mice, the predominantly produced antibody became Th2-associated antibody IgG1 [65]. In the study by He et al., Th1 cells were highly activated when Th2-associated cytokine IL-10 knockout DC was stimulated and adoptively transferred [67]. In another related study, Lu and Zhong incubated bone marrow-derived DCs with heat-killed *C. trachomatis* and showed that a Th1 response developed after nasal infection of mice with live *C. trachomatis* [68]. DCs provide a link between innate and adaptive immunity in the control of chlamydial infection. Chlamydiae limit MHC class I/II expression in antigen presenting cells to cope with the immune response at this stage [69]. Chlamydial protease-activating factor (CPAF) released into the cytogel by *C. trachomatis* has been shown to inhibit MHC molecules by degrading the MHC class I transcription factor RFX-5 and the MHC class II transcription factor USF-1 [70, 71].
