The activation of T helper cells by APC causes them to differentiate into different subtypes with specic functions mediated by cytokine secretion and cell-to-cell contact. T helper 1 cells secrete cytokines such as IFN-γ, IL-6, and IL-12 and play a crucial role in cellular response formation [15]. Th2 cells help humoral responses by providing a second signal to B cells, mostly through IL-4 secretion and CD40/ CD40L interaction. During the rst encounter with an antigen (pathogen), long­lived memory T and B cells are established. In subsequent encounters with the same pathogen, the memory cells are quickly activated to yield a more rapid and robust protective response. The activated B cells secrete antibodies circulating in the body and coat the microbes, targeting them for efcient phagocytosis. T follicular helper cells (Tfh) control the critical interactions in the germinal centers essential for the maturation of memory B cells and long-lived high-afnity antibody-producing plasma cells [31]. Another subset of CD4+ T cells differentiates into a pool of mem­ory T helper cells. Activated CD8+ cytotoxic T lymphocytes (CTL) cause apoptosis of the infected host cells. Some CTLs differentiate into memory cytotoxic T cells, which have the role of fast restoration of the CTL response with secondary antigen contacts. A similar destruction mechanism occurs when NK cells interact with the virally infected cell [31]. They contain granules with IFN-γ and TNF-α in their cytoplasm. NK cells form pores in the membranes of target cells by perforin. Granzymes pass through the pores, and together with cytokines, they initiate apop­tosis, resulting in the death of infected cells.