Table 4.
Cytokines used in diagnosis and chemo/immunotherapy of VL.
| Cytokine | Relative functions in leishmaniasis | References |
|---|---|---|
| Anti-IL-10R | Controls the experimental VL and induces antimonials activity in IL-10 knock-out or transgenic mice and IFN-γ production | (53, 56) |
| IL-10 | Neutralization increases IFN-γ and TNF-α production and reduces parasite burden in VL patients | (187) |
| Abundant in antigen-stimulated PBMCs of L. chagasi infection | ||
| In asymptomatic individuals, IL-10 not directly correlates with Montenegro test positivity | (188) | |
| Balanced IL-10 and IL-12 response induces chemotherapy efficacy | (17) | |
| Disease relapse in human VL associates with IL-10 and IL-10+IFN-γ+ antigen-specific T-cells | (189) | |
| Clinical symptoms strongly correlates with IL-6, IL-27, TNF-α, and IL-10 in L. infantum infected Brazilian population | (190) | |
| IL-4 | Upregulates in VL and associates with impaired treatment | (191, 192) |
| IFN-γ, IL-4, and IL-13 certainly upregulates in active VL and declines after cure | (193) | |
| IFN-γ | Absence of antigen-specific lymphocyte proliferation and IFN-γ production indicates clinical disease | (45) |
| Useful in assessing candidacy of vaccine antigens | (194) | |
| Sbv with rIFN-γ had shown 82.3, 75, and 87% efficacy against VL patients from Brazil, Kenya, and India, respectively | (195–197) | |
| IL-12 | Induces better response than anti-IL-10 alone or in combination with anti-IL-4 from PBMCs of VL patients | (115) |
| VL cure restores the IFN-γ and IL-12 production | (48) | |
| Useful as effective adjuvant for a killed vaccine against L. major | (198) | |
| rIL-12 mediates the cure of L. major infection, induces Th1 cytokines and inhibits IL-4 | (75, 81, 200) | |
| Neutralization exacerbates L. major and L. donovani infections | (49, 69, 199) | |
| IL-15 | Liposomal amphotericin-B induces plasma IL-15 levels in VL | (86) |
| IL-15 with combination of IFN-γ or IL-12 increases efficacy of antimonial therapy for VL | (201) | |
| TNF-α | Anti-TNF-α therapy for arthritis increases susceptibility to VL | (202, 203) |
| In HIV co-infection, high levels of serum TNF-α and IFN-γ predicts the onset of acute VL | (204) | |
| TGF-β & IL-13 | Antagonists of these clears the VL marginally and had no synergy with SbV | (119) |