Abstract
T cell migration is crucial for an effective adaptive immune response to invading pathogens. Naive and memory T cells encounter pathogen antigens, become activated, and differentiate into effector cells in secondary lymphoid tissues, and then migrate to the site(s) of infection where they exert effector activities that control and eliminate pathogens. To achieve activation, efficient effector function, and good memory formation, T cells must traffic between lymphoid and non-lymphoid tissues within the body. This complex process is facilitated by chemokine receptors, selectins, CD44, and integrins that mediate the interactions of T cells with the environment. The expression patterns of these migration receptors (MR) dictate the tissues into which the effector T cells migrate and enable them to occupy specific niches within the tissue. While MR have been considered primarily to facilitate cell movement, we highlight how the heterogeneity of signaling through these receptors influences the function and fate of T cells in situ. We explore what drives MR expression heterogeneity, how this affects migration, and how this impacts T cell effector function and memory formation.
Highlights
In this review, we focus on T cell heterogeneity defined as the variation in the expression of migration receptors (MR), including chemokine receptors (CCRs), selectins, CD44, and integrins
CD4+ and CD8+ T cells are heterogeneous and subsets have been defined based on the expression of CCRs, selectins, and integrins that are able to engage inflamed endothelium, the extracellular matrix (ECM), and cells of the innate immune system
For effector T cells that relocate to sites of inflammation, considerable plasticity in their responses can occur during the priming process with dendritic cells (DC) that imparts a tissuespecific MR phenotype to ensure efficient homing of activated T cells to the correct tissue
Summary
We focus on T cell heterogeneity defined as the variation in the expression of migration receptors (MR), including chemokine receptors (CCRs), selectins, CD44, and integrins. A functional T cell response is a crucial component of effective immunity to infection with pathogens and is influenced by a multitude of factors that include the microbe-specific mechanisms of host engagement, the site(s) of entry, and the virulence of the pathogen. Control and/or clearance depends upon the effector activities of CD8+ and CD4+ T cells that are programed to mediate type I responses characterized by cytolytic activity and production of cytokines, such as interferon (IFN)-γ and tumor necrosis factor (TNF)-α. These responses are initiated primarily by antigen-presenting DC that have migrated from the site of infection to the secondary lymphoid organs (SLO). For naïve T cells, it is well-established that L-selectin (CD62L), CCR7, and LFA (CD18, β2) are the key molecules that regulate entry into LNs, which occurs through high endothelial venules that present their respective ligands, PNAd, CCL21, and ICAM-1
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