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The canine adaptive immune system is a sophisticated biological network in dogs responsible for pathogen-specific defense and the establishment of immunological memory, primarily mediated by B-lymphocytes and T-lymphocytes (Day, 2010). It functions by recognizing unique antigens via highly diverse receptors, leading to clonal expansion and the production of specific antibodies or cell-mediated cytotoxic responses. This system plays a critical role in the pathogenesis of numerous canine diseases, including atopic dermatitis, immune-mediated hemolytic anemia (IMHA), and various lymphoid malignancies (Gershwin, 2018). Therapeutic strategies in veterinary medicine often target this system to either suppress unwanted immune responses in autoimmune and allergic conditions or to stimulate anti-tumor activity in oncology. However, broad pharmacological modulation of the adaptive immune system carries significant risks, such as increased vulnerability to opportunistic infections and a potential reduction in the efficacy of routine vaccinations (Oliveira et al., 2019).
Therapeutic modulation of the canine adaptive immune system involves diverse mechanisms such as the inhibition of Janus kinase (JAK) pathways to block cytokine signaling (e.g., oclacitinib), the inhibition of calcineurin to suppress T-lymphocyte activation (e.g., cyclosporine), and the use of monoclonal antibodies to neutralize specific interleukins like IL-31 (e.g., lokivetmab) (Gadeyne et al., 2014; Gonzales et al., 2013).
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