Abstract
The term “immune synapse” was originally coined to highlight the similarities between the synaptic contacts between neurons in the central nervous system and the cognate, antigen-dependent interactions between T cells and antigen-presenting cells. Here, instead of offering a comprehensive molecular catalogue of molecules involved in the establishment, stabilization, function, and resolution of the immune synapse, we follow a spatiotemporal timeline that begins at the initiation of exploratory contacts between the T cell and the antigen-presenting cell and ends with the termination of the contact. We focus on specific aspects that distinguish synapses established by cytotoxic and T helper cells as well as unresolved issues and controversies regarding the formation of this intercellular structure.
Highlights
The immune synapse (IS) is a central event in the development of the adaptive immune response that results in the activation of the T cell
The “synapse-like” nature of the intimate contact between the T cell and the antigen-presenting cell (APC) during T cell activation was initially proposed by Norcross in the early 1980s1, the term “immunological synapse” first appeared in a review by Paul and Seder in 19942
The IS can be defined as a stimulus-driven, spatiotemporal segregation of molecules that participate in T cell activation
Summary
The immune synapse (IS) is a central event in the development of the adaptive immune response that results in the activation of the T cell. There is evidence of small (nanosized) TCR clusters even before their interaction with the MHC These nanoclusters are continually generated throughout the plasma membrane of the T cell[24] and migrate and coalesce at the center of the contact to form micron-scale structures, termed central Supramolecular Activation Clusters (cSMACs) (Figure 1, top)[25], which concentrate signaling components (reviewed in 26) as well as molecules involved in co-stimulation, e.g. CD2827. Formation of a secretory domain in the CTL synapse Actin accumulation at the IS facilitates the initial activation of the T cell by immobilizing receptors involved in the contact with the APC and sustaining localized signaling. It constitutes a steric hindrance for polarized secretion. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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