Phenotypic markers associated with antigen-induced differentiation of naive CD8⁺ T cells. Within 48 hours after TCR activation, naive and memory CD8⁺ T cells up-regulate activation markers including IL-2R, Ki67, PCNA, and respond to signals delivered through JAK/STAT pathways to undergo changes in chemokine and homing receptors. CD62L is down-regulated and cleaved from the cell surface and IL-7Rα (CD127) expression is lost. During the proliferative phase a small subset of cells defined as memory precursor effector cells (MPECs) reacquire the IL-7Rα and have the potential to persist into long-term memory whereas the population that fails to up-regulate this receptor represent short-lived effector cells (SLECs).^26,27,37  The antigen-specific T-cell population that fails to up-regulate IL-7R expresses high levels of killer cell lectin-like receptor G1 (KLRG1). Although all antigen-activated CD8⁺ T cells are thought to express immediate effector function and proliferative capacity, transition to memory is dependent upon multiple sequential signals received by the T cell including the intensity and duration of TCR activation, CD4⁺-proficient help, costimulation, and cytokines that regulate survival. Transition to memory after natural infection is more dependent on IL-7, whereas T cells that receive weaker signals in the case of soluble protein antigens delivered with adjuvants are equally dependent on IL-7 and IL-15 for survival and transition to memory. Defining phenotypic and functional markers that characterize different transitional phases of CD8⁺ T cells induced by different viral vectors and other delivery systems will be instrumental in advancing strategies for effective T-cell vaccines for HIV-1, cancer, and other infectious diseases. CD45RA also known as leukocyte common antigen, highly glycosylated protein tyrosine phosphatase regulating TCR, BCR activation and found on naive/resting T cells; CD44, family of cell-surface glycoproteins involved in leukocyte attachment and rolling on endothelial cells and homing to peripheral lymphoid organs by binding mucosal addressin on high endothelial venules. Marker for antigen-experienced cells; CCR7, CC-chemokine G protein–coupled receptor guides cells from peripheral tissue into lymph nodes binding CCL19 (Mip3β) and CCL21(SLC) deposited on HEVs and reticular network; CD62L, L-selectin binds to CD34 and mediates lymphocyte homing through high endothelial venules of peripheral lymphoid tissue and inflamed tissue; CD127, also known as IL-7R; CD122, (IL-2β chain) pairs with γ common chain. Critical component of IL-2 and IL-15–mediated signaling; CD28, constitutive, low-affinity costimulatory signal induces T-cell activation, IL-2 production, and survival; CD27, TNFR superfamily member 7 binds to CD70. Costimulatory signal helps differentiate memory-type CD8⁺ T cells (CD27⁺) from effector-type CD8⁺ T cells (CD27⁻); CD43, leukosialin ligand-receptor complex involved in T-cell activation. Ligand for E-selectin and may regulate T-cell trafficking; CD95, TNF receptor superfamily member 6 also known as Fas. Cell-surface membrane receptor that activates apoptotic pathways when bound by Fas ligand (FasL, CD178); KLRG1, killer cell lectin-like receptor G1, senescence-associated inhibitory receptor binds E cadherin and inhibits AKT phosphorylation; Perforin, is indispensable for granule-mediated cell death by CD8⁺ CTL; Granzyme B, serine protease–inducing caspase-dependent apoptosis. Performs a key role in the cytotoxic activity mediated by CD8⁺ CTL (http://www.pathologyoutlines.com/cd100247.html).