**2.2 Type III secretion systems**

Intracellular pathogens secrete contact-dependent protein products of conserved secretory genes [3]. Those proteins promote the viability and multiplication of the microbe within the host cell and are well-described virulence factors. Their role is to intercept host signaling pathways in favor of the intruder [3]. Type III secretion systems serve as a conduit to promote the delivery of pathogen-effector proteins into the cytoplasm of the host cell. Via this apparatus, the microorganism can inject proteins directly into the host cell and avoid lysosomes [10]. *Chlamydiae* have a unique life cycle where the elementary body is metabolically dormant and therefore expresses no contact secretion. This contrasts with other intracellular pathogens, where contact-dependent secretion begins before they have been internalized in the host cell [3]. In *Chlamydiae* contact secretion is triggered from within by the intracellular metabolically active reticulate body. Therefore, characterization and description of *Chlamydiae* contact-dependent secretion mechanisms are of great interest [3]. The product of *scc1* gene has homology to chaperone proteins of other intracellular pathogens. *Cds1 and cds2* locuses are acquired by horizontal transfer and thus are included in a classical pathogenicity island. They are expressed during the intracellular life cycle of the bacterium and are related to the translocation of the pathogen across the cytoplasmic membrane [3]. Effector protein IncA of *C. trachomatis* mediates inclusion fusion and is related to strain-dependent disease severity [10]. Another chlamydial phosphoprotein is delivered into host cell cytoplasm and promotes actin recruitment in favor of the pathogen. This so-called Translocated Actin Recruiting Phosphoprotein causes internalization of the microbe and is related to disease severity [10, 11].
