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Open AccessJournal ArticleDOI

Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens.

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TLDR
It is suggested that SAgs can act as targeted modulators that drive the immune response away from an effective response, and thus aid in S. aureus persistence.
Abstract
Staphylococcal superantigens (SAgs) constitute a family of potent exotoxins secreted by Staphylococcus aureus and other select staphylococcal species. SAgs function to cross-link major histocompatibility complex (MHC) class II molecules with T cell receptors (TCRs) to stimulate the uncontrolled activation of T lymphocytes, potentially leading to severe human illnesses such as toxic shock syndrome. The ubiquity of SAgs in clinical S. aureus isolates suggests that they likely make an important contribution to the evolutionary fitness of S. aureus. Although the apparent redundancy of SAgs in S. aureus has not been explained, the high level of sequence diversity within this toxin family may allow for SAgs to recognize an assorted range of TCR and MHC class II molecules, as well as aid in the avoidance of humoral immunity. Herein, we outline the major diseases associated with the staphylococcal SAgs and how a dysregulated immune system may contribute to pathology. We then highlight recent research that considers the importance of SAgs in the pathogenesis of S. aureus infections, demonstrating that SAgs are more than simply an immunological diversion. We suggest that SAgs can act as targeted modulators that drive the immune response away from an effective response, and thus aid in S. aureus persistence.

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Citations
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Adult chronic rhinosinusitis.

TL;DR: The introduction of endotyping has led to a differentiation of ‘tailored’ surgical approaches, focusing on the mucosal concept in those with severe CRSwNP and on the identification of patients eligible for extended surgery and possibly biologics in the future.
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HLA class I-associated expansion of TRBV11-2 T cells in Multisystem Inflammatory Syndrome in Children.

TL;DR: In this article, the authors characterized the TCR repertoire of multisystem inflammatory syndrome in children (MIS-C), a hyperinflammatory syndrome associated with SARS-CoV-2 infection, and found a profound expansion of TCRβ variable gene 11-2, with up to 24% of clonal T cell space occupied by TRBV11-2 T cells, which correlated with MIS-C severity and serum cytokine levels.
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Staphylococcus aureus bloodstream infections: pathogenesis and regulatory mechanisms.

TL;DR: The current understanding of the pathogenesis of these invasive infections is presented, focusing on the mechanisms of S. aureus clearance from the bloodstream by the immune system, and how this pathogen hijacks the host defense and coagulation systems and further interacts with the blood vessel endothelium.
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Staphylococcal Superantigens: Pyrogenic Toxins Induce Toxic Shock.

TL;DR: The induction of these damage response genes provides evidence that SEB induces danger signals in host cells, resulting in multiorgan injury and toxic shock, andTherapeutics targeting both host inflammatory and cell death pathways can potentially mitigate the toxic effects of staphylococcal superantigens.
Journal ArticleDOI

Staphylococcus aureus Exotoxins and Their Detection in the Dairy Industry and Mastitis

TL;DR: The role of S. aureus toxins in the development of mastitis in ruminants, their negative effects in the food and dairy industries, and the different methods used for the identification of these toxins in food destined for human consumption are summarized.
References
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Journal ArticleDOI

Myeloid-derived suppressor cells as regulators of the immune system.

TL;DR: The origin, mechanisms of expansion and suppressive functions of MDSCs, as well as the potential to target these cells for therapeutic benefit are discussed.
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Staphylococcus aureus Infections: Epidemiology, Pathophysiology, Clinical Manifestations, and Management

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Journal ArticleDOI

Immune evasion by staphylococci

TL;DR: Staphylococcus aureus can cause superficial skin infections and, occasionally, deep-seated infections that entail spread through the blood stream, and must rely primarily on cell-surface polymers and the ability to form a biolfilm to survive in the host.
Journal ArticleDOI

Temporal Dynamics of the Human Vaginal Microbiota

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