Table 1.
Cytokines involve in the host protection.
| Cytokine | Relative functions in leishmaniasis | References |
|---|---|---|
| IFN-γ | Activates MΦs and monocytes to release oxygen radicals and TNF-α, IL-l, and IL-6 secretion Blocks the production of IL-10 | (63–67) |
| Absence leads to Th2 skewing | (48) | |
| IL-12 | Drives Th1 response and IFN-γ production | (68) |
| Controls Th2 expansion and IL-4 production | (69, 70) | |
| Induces NOS2 expression and NO production | (71) | |
| Induces cell proliferation and lymphokines production | (71, 72) | |
| TNF-α | Activates the MΦs to kill amastigotes | (73) |
| Induces NO production to kill the parasite or inhibit visceralization | (74) | |
| Induces granuloma response and wound healing process | (75, 76) | |
| Shows IFN-γ-independent leishmanicidal activity | (77, 199) | |
| Promotes IL-10 producing T-cells for immune homeostasis | (78) | |
| IL-2 | Activates T-cells and NK cells and induces IFN-γ production | (79, 80) |
| Induces the production of IL-4 | (81) | |
| Endogenous IL-2 shows host protection | (82) | |
| Exogenous IL-2 exerts anti-leishmanial action even in the absence of IFN-γ | (83) | |
| IL-15 | Synergizes with IL-2 and IL-12 functions | (84, 85) |
| Induces T-cell proliferation and inhibits apoptosis, preserves memory T-cells, and induces B-cell maturation and isotype switching | (86–88) | |
| Activates both Th1 and Th2 subtypes and shows pleiotropic role | (89, 90) | |
| Stimulates Th1 response, IL-12 production and downregulates IL-4+ Th2 cells | (86, 91) | |
| IL-22 | Promotes inflammatory response and is crucial in tissue repair | (92, 93) |
| Protects the liver from chronic infections | (94) | |
| Induces the production of antimicrobial peptide-β-defensin | (95) | |
| Complementary to Th1 cytokines and requires IL-6 for production | (96–98) | |
| IL-7 | Induces proliferation of thymocytes, NK and mature T-cells, and production of cytotoxic T-cells | (99–104) |
| Promotes the synthesis and secretion of IL-6, TNF-α, IL-1α, IL-1β, and MIP-113 by monocytes | ||
| With the combination of IFN-γ, it induces TNF-α and NO production to kill the amastigotes | (105) | |
| IL-8 | Promotes the recruitment of neutrophils and granulocytes at lesion site | (106, 107) |
| Declines in the serum of active VL and polymorphism at −251 position associates with active VL | (32, 108) | |
| IL-23 | Shows IL-12 independent protection against visceral infection | (76, 109, 110) |
| P19 pairs with IL-12p40 to become active and protects the host | (111) |