01971nas a2200229   4500000000100000008004100001260001200042653001500054653000900069653002200078653000900100653001800109653001600127100002000143700001300163245009200176856006300268300000900331490000800340520137900348022001401727       2026                            d  c03/202610aLeishmania10aCD1d10aT‐cell receptor10aiNKT10aLeishmaniasis10aα‐GalCer1 aBandyopadhyay S1 aPandey S00aThe Enigma of CD1d-iNKT Axis in Leishmaniases: Current Insights Into Immune Regulation.  uhttps://onlinelibrary.wiley.com/doi/epdf/10.1111/sji.70102  a1-210 v1033 a<p>Leishmaniases caused by Leishmania parasites may be fatal if proper treatment is lacking. These protozoan parasites employ several strategies to control the host immune system. Among these, manipulation of the antigen presentation pathway is crucial for survival in the host. In addition to protein antigens produced by Leishmania sp. parasite-derived lipid or glycolipid antigens are known which are potentially important at the interface of host-parasite interactions. CD1d is a cell surface-expressed receptor that presents both endogenous and exogenous lipids and glycolipids to the TCR of invariant NKT cells. The CD1d-iNKT axis is important during the initial stages of infection by several species of Leishmania, although it may not be required for resolution of the infection at a later stage in mice. Owing to the limited number of published reports, heterogeneity in response is evident in both mice and human. Organ-specific, host species-specific and parasite species-specific responses make the concept even more complex. In this review, we comprehensively summarise the role of the CD1d-iNKT axis in the regulation of Leishmania infection. A deeper understanding of the mechanistic role of the CD1d-iNKT axis during Leishmania infection in human may provide a foundation for the rational design of targeted immunotherapeutic interventions in the future.</p>  a1365-3083