Background: Leishmaniasis is an infection transmitted by arthropod vectors and is caused by protozoan parasites of the genus Leishmania. Primarily, dogs function as reservoirs. Emerging evidence points to cats as secondary hosts. This study aimed to review innate immune responses and parasite evasion mechanisms in canine and feline leishmaniasis.
Methods: This narrative review synthesized peer-reviewed studies on innate immune responses to Leishmania infection in dogs and cats, identified through searches of major biomedical databases (including PubMed, Scopus, and Web of Science) from 1990 to 2025. Eligible articles reported immunological data on innate cells, cytokine profiles, or parasite evasion; non-English publications, case reports, and studies without immune outcomes were excluded. Key findings were qualitatively integrated to compare species-specific responses and associated clinical outcomes.
Results: Dogs with progressive disease show mixed Th1-Th2 responses, with IL-10 and TGF-β promoting parasite persistence. Cats more often exhibit dominant Th1 responses, with elevated IL-12 and IFN-γ correlating with greater suppression of parasite growth and subclinical infection. Leishmania evades immunity by inhibiting phagolysosome maturation, modulating Toll-like receptor signaling, and suppressing reactive oxygen and nitrogen species. Cats display lower antibody production than dogs, contributing to their resistance; however, co-infections with retroviruses increase feline susceptibility. -12/IFN-γ-inducing vaccines and therapies targeting IL-10/TGF-β pathways show potential.
Conclusion: Distinct innate immune responses shape disease outcomes in dogs and cats, necessitating tailored diagnostic and therapeutic approaches and inclusion of feline leishmaniasis in One Health surveillance.