Fig. 1

Model of immune response to different classes of pathogens. The pathogen is taken up by an antigen-presenting cell (APC) following interactions between antigenic motifs on the pathogen and pattern recogniton receptors expressed by the APC. The pathogen is processed and pathogen-derived antigenic peptides are expressed on the surface of the APC in association with molecules of the major histocompatibility complex (MHC). The T-cell receptor (TCR) of a naïve T lymphocyte recognizes the MHC-peptide complex and the cell receives costimulatory cytokine and surface molecular signals from the APC. The naïve T cell differentiates down one of the pathways of CD4⁺ T cell development as determined by signalling from the APC. T helper 1 (Th1) cells produce interferon (IFN)-γ and direct cell-mediated immunity (CMI) to intracellular pathogens (e.g. viruses, mycobacteria and many arthropod-borne microparasites). Th2 cells produce interleukin (IL)-4, IL-5 and IL-13 and direct antibody responses (humoral immunity) to extracellular pathogens. Th17 cells produce IL-17A, IL-17 F and IL-22 and respond to fungal infections by mobilizing neutrophils. T follicular helper (T_FH) cells produce IL-21 and lead to establishment of long-term protective humoral immunity via generation of high-affinity antibodies. In contrast to all of the preceding cells, which have a positive action in antimicrobial defence (effector T cells), regulatory T cells (Treg) produce IL-10 and are responsible for down-regulation of immune responses; sometimes in balance with effector T cells to achieve non-sterilizing immunity allowing an animal to be infected, but without significant clinicopathological effect. The balance between the activity of these cells determines the outcome to infection, and in the context of this review, it might be that dogs and cats have a different balance between these cells within their immune responses