Abstract
The human body frequently encounters harmful bacterial pathogens and employs immune defense mechanisms designed to counteract such pathogenic assault. In the adaptive immune system, major histocompatibility complex (MHC)-restricted αβ T cells, along with unconventional αβ or γδ T cells, respond to bacterial antigens to orchestrate persisting protective immune responses and generate immunological memory. Research in the past ten years accelerated our knowledge of how T cells recognize bacterial antigens and how many bacterial species have evolved mechanisms to evade host antimicrobial immune responses. Such escape mechanisms act to corrupt the crosstalk between innate and adaptive immunity, potentially tipping the balance of host immune responses toward pathological rather than protective. This review examines the latest developments in our knowledge of how T cell immunity responds to bacterial pathogens and evaluates some of the mechanisms that pathogenic bacteria use to evade such T cell immunosurveillance, to promote virulence and survival in the host.
Highlights
The human body has evolved a complex symbiotic relationship with innocuous, commensal bacteria in which immunological defense mechanisms are tempered, to allow a state of mutualism that is beneficial to both the host and the colonizing microbiota
major histocompatibility complex (MHC)-restricted αβ CD4+ and CD8+ T cells, provide immune defense in response to peptidic antigens, whilst unconventional αβ (MAIT cells, CD1-restricted T cells) and γδ T cells, utilize MR1, CD1 molecules and BTN/BTNL molecules to respond to lipidic, metabolic, or undiscovered antigens of bacterial origin
In the case of γδ T cells, the process of identifying γδ T cell antigens is complicated and, as such, the nature of bonafide antigens that respond to γδ T cell receptors (TCRs) is largely unclear [26]
Summary
The human body has evolved a complex symbiotic relationship with innocuous, commensal bacteria in which immunological defense mechanisms are tempered, to allow a state of mutualism that is beneficial to both the host and the colonizing microbiota. Αβ T cells can respond to structurally different antigens (e.g., lipids, metabolites) presented by non-polymorphic MHC-like molecules, such as MHC class I-related gene protein (MR1) and CD1 glycoproteins [22,23,24,25] Such “unconventional” T cell populations (Figure 1), including mucosal-associated invariant T (MAIT) cells and invariant natural killer T (iNKT) cells, appear to be “innate-like”, as they are poised to respond faster than T cells restricted by classical MHC molecules and display invariance in their TCR repertoire, which limits their clonotypic diversity [24]. HmouwniTtyCtoelblsacFtiegrhiatlBpaacttheorgiaens and evaluates the mechanisms bacteria use to evade such T cell immunosurveillance
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