Figure 3.

Visual summary of key T_RM effector responses and vaccine strategies at epithelial surfaces. (A) Represents the female reproductive tract. Topical application of both specific chemokines and general inflammatory agents such as nonoxynol-9 can be used to “pull” systemically primed T_EM into the mucosal tissue. CD103⁺ T_RM reside closer toward the apical surface of the mucosa. Both CD4⁺ and CD8⁺ T_RM play a role in controlling viral infections. Memory lymphocyte clusters have been shown to be important in controlling infections at this site. CD8⁺ T_RM re-stimulation appears to be dependent on CD301b⁺ dendritic cells that reside in the lamina propria. (B) Represent the integumentary epithelium. Topical application of both specific chemokines and general inflammatory agents such as 2,4-dinitroflourobenzene can be used to “pull” systemically primed T_EM into the epidermal tissue. Skin scarification as a route of vaccination encourages the development of skin T_RM. Upon antigen recognition, skin T_RM lose their dendricity and become less motile. γδ T_RM can mediate early immune responses. CD8⁺ αα⁺ T_RM have been found in the dermal–epidermal junction where they may be able to survey local neural tissue for reactivation of latent viral infections. (C) Represents the respiratory epithelium. While different chemokines have shown the ability to “pull” T_RM into the respiratory epithelium and airways, the presence of antigen appears to be important at this site. T_RM-mediated control of Streptococcus pneumoniae is largely dependent on the CD4⁺ subset. Control of viral and Mycobacterium tuberculosis infection requires both CD4⁺ and CD8⁺ T_RM. γδ T_RM, in conjunction with CD4⁺ T_RM have been shown to mediate immunity against Bordetella pertussis.