**5.3 IFN-γ-induced persistence**

IFN-γ is the major component of the innate immune response against *Chlamydia* and is the factor that has received the most research attention as a Chlamydial inducer of persistence [41, 43, 44, 67]. Various mechanisms of IFN-γ-induced persistence have been proposed. IFN-γ activates the catabolic depletion of L-tryptophan (Trp) via indoleamine-2,3-dioxygenase (IDO), the enzyme that degrades tryptophan. Since tryptophan is an essential amino acid for *C. trachomatis*, the presence of this enzyme induces a tryptophan starvation that inhibits the growth of Chlamydial RBs [41, 43]. IFN-γ is also involved in the inhibition of the transcription factor and proto-oncogene c-Myc, the key regulator of host cell metabolism and a central regulator of *Chlamydia* persistence [67].

#### **5.4 Autophagy: mediated resistance**

Autophagy is a physiological degradation process that occurs within the lysosomes of most cell types. Its main functions are to maintain cellular homeostasis and selectively remove intracellular bacteria or viruses. In *C. trachomatis*, Guanylate-binding proteins (GBPs) and the immunity-related GTPases (IRGs) such as GBP1, GBP2, Irga6, and Irgd, which can induce lysis and infection clearance by autophagy, were found to accumulate in the *Chlamydial* inclusions [68, 69], suggesting a role for these proteins in the autophagy-mediated resistance to *C. trachomatis* infection.
