Fig. 1.

Schematic model showing the mechanism by which Sema3E protects against chlamydial infection. Chlamydial lung infection induces the production of Sema3E. Sema3E binds to its receptor, plexinD1, expressed on DCs, thus upregulating co-stimulatory molecules, chemokine receptor (CCR7), and IL-12 cytokine production. Sema3E modulated DC migrate to the draining lymph nodes and promotes Th1/Th17 response and inhibits Th2 and Treg response. The modulated DC can also promote IgG2a antibody production. These responses result in the clearance of Chlamydia (Thomas et al., 2021), (Thomas et al., 2022).