The Immunological Synapse: An Emerging Target for Immune Evasion by Bacterial Pathogens

Abstract

Similar to other pathogens, bacteria have developed during their evolution a variety of mechanisms to overcome both innate and acquired immunity, accounting for their ability to cause disease or chronic infections. The mechanisms exploited for this critical function act by targeting conserved structures or pathways that regulate the host immune response. A strategic potential target is the immunological synapse (IS), a highly specialized structure that forms at the interface between antigen presenting cells (APC) and T lymphocytes and is required for the establishment of an effective T cell response to the infectious agent and for the development of long-lasting T cell memory. While a variety of bacterial pathogens are known to impair or subvert cellular processes essential for antigen processing and presentation, on which IS assembly depends, it is only recently that the possibility that IS may be a direct target of bacterial virulence factors has been considered. Emerging evidence strongly supports this notion, highlighting IS targeting as a powerful, novel means of immune evasion by bacterial pathogens. In this review we will present a brief overview of the mechanisms used by bacteria to affect IS assembly by targeting APCs. We will then summarize what has emerged from the current handful of studies that have addressed the direct impact of bacterial virulence factors on IS assembly in T cells and, based on the strategic cellular processes targeted by these factors in other cell types, highlight potential IS-related vulnerabilities that could be exploited by these pathogens to evade T cell mediated immunity.

Sleep Restriction Modulates B‐1 Cell Response Following Fungal Infection

“…In the present study, the sleep restriction no influence the expression of costimulatory molecules in B-1 cells, except for the marker CD86, which was less expressed after inoculation with C. albicans. CD86 is a costimulatory molecule that binds to the CD28 receptor on T lymphocytes, leading to a T cell-mediated immune response (reviewed by [28]). The observation that the expression of this molecule is reduced in sleep-restricted mice following infection with C. albicans suggests a potential association with fungal components rather than solely with sleep restriction.…”

Understanding bacterial pathogenicity: a closer look at the journey of harmful microbes

“…Bacterial virulence factors modulate the immune synapse, aiding the bacteria in evading the immune mechanisms of host cells. This unique aspect of adaptive immunity lies in its ability to establish a memory, enabling a swifter and more efficient immune response upon re-exposure to the antigen (Capitani and Baldari, 2022 ).…”

Rab GTPases, Active Members in Antigen‐Presenting Cells, and T Lymphocytes

“…The interaction between these two systems lies in the mobilization of antigens through the complex endocytic network to the cell–cell contact interface [147]. When a microorganism is phagocytosed, it is mobilized and processed in several specific compartments (associated with different Rab GTPases) and then transported to the cell surface in association with molecules of the major histocompatibility complex and presented to T cells within the immune synapse [148]. It is important to mention that the spatial organization of the three‐dimensional endocytic network actively participates in the availability and distribution of antigens and that this is regulated by an adequate interaction between the various intracellular membranous compartments and the plasma membrane, allowing the optimization of the activation of T cells [149].…”