Leishmania infantum-specific IFN-? production in stimulated blood from cats living in areas where canine leishmaniosis is endemic

Priolo, Vito; Martínez-Orellana, Pamela; Pennisi, Maria Grazia; Masucci, Marisa; Prandi, David; Ippolito, Dorotea; Bruno, Federica; Castelli, Germano; Solano-Gallego, Laia

Feline leishmaniosis (FeL) due to L. infantum infection was described, for the first time, in 1912 by Sergent et al. [6] and since then it has been globally reported in endemic areas [5, 7] . While subclinical feline infections are common in areas where canine leishmaniosis (CanL) is endemic, clinical illness due to FeL is rare [7, 8] . Clinical disease is frequently associated with possible impaired immunocompetence, as in case of retroviral co-infections, immunosuppressive therapy, or malignant neoplasia [7, 8] . The immune response plays a crucial role in the control of Leishmania infection. Albeit some differences according to the host species, T cells modulate and orient, through cytokine production, macrophage reaction to the parasite [9] [10] [11] . Antigen processing cells (dendritic cells and macrophages) present L. infantum antigens to CD4 + T cells that modulate the type of immune response [12] . A T helper 1 (Th1) oriented immune response, associated with production of interferon-gamma (IFN-γ), interleukin (IL)-2 and tumor necrosis factor alpha (TNFα), stimulates phagocytosis by macrophages, their production of nitric oxide and reactive oxygen intermediate and consequent phagocyte-based parasite intracellular elimination [11, 13] . Conversely, in dogs susceptibility to infection and disease progression is mediated predominantly by a non-protective T helper 2 (Th2) immune response and the production of cytokines such as IL-4, IL-10, IL-13 and transforming growth factor beta (TGFβ) which are associated with downregulation of the cellular immune response, a high level of antibodies, and L. infantum dissemination [9] [10] [11] .