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| http://dx.doi.org/10.1128/iai.58.8.2409-2413.1990 | DOI Listing |
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Novel insights into the immune response to bacterial T cell superantigens.
Nat Rev Immunol
June 2024
Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada.
Bacterial T cell superantigens (SAgs) are a family of microbial exotoxins that function to activate large numbers of T cells simultaneously. SAgs activate T cells by direct binding and crosslinking of the lateral regions of MHC class II molecules on antigen-presenting cells with T cell receptors (TCRs) on T cells; these interactions alter the normal TCR-peptide-MHC class II architecture to activate T cells in a manner that is independent of the antigen specificity of the TCR. SAgs have well-recognized, central roles in human diseases such as toxic shock syndrome and scarlet fever through their quantitative effects on the T cell response; in addition, numerous other consequences of SAg-driven T cell activation are now being recognized, including direct roles in the pathogenesis of endocarditis, bloodstream infections, skin disease and pharyngitis.
View Article and Find Full Text PDFInnate TCRβ-chain engagement drives human T cells toward distinct memory-like effector phenotypes with immunotherapeutic potentials.
Sci Adv
December 2023
Peter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College London, London, SE1 9RT, UK.
Clonotypic αβ T cell responses to cargoes presented by major histocompatibility complex (MHC), MR1, or CD1 proteins underpin adaptive immunity. Those responses are mostly mediated by complementarity-determining region 3 motifs created by quasi-random T cell receptor (TCR) gene rearrangements, with diversity being highest for TCRγδ. Nonetheless, TCRγδ also displays nonclonotypic innate responsiveness following engagement of germline-encoded Vγ-specific residues by butyrophilin (BTN) or BTN-like (BTNL) proteins that uniquely mediate γδ T cell subset selection.
View Article and Find Full Text PDFThe influence of variable-heavy chain families on IgG, , , FcγRs and B-cell superantigens protein G and L binding using biolayer interferometry.
Antib Ther
July 2023
Antibody& Product Development Lab, Agency for Science, Technology and Research (A*STAR), Singapore, and Wenzhou-Kean University, Wenzhou, Zhejiang, China.
As the most abundant immunoglobulin in blood and the most common human isotype used for therapeutic monoclonal antibodies, the engagement and activation of its Fc receptors by IgGs are crucial for antibody function. Assumed to be relatively constant within subtypes, recent studies reveal that antibody variable regions exert distal effects of modulating antibody-receptor interactions on antibody isotypes. These variable (V)-region distal effects are also expected for the IgG subtypes.
View Article and Find Full Text PDFThe homodimer interfaces of costimulatory receptors B7 and CD28 control their engagement and pro-inflammatory signaling.
J Biomed Sci
June 2023
Department of Biochemistry and Molecular Biology, Institute of Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, 9112102, Jerusalem, Israel.
Background: The inflammatory response is indispensable for protective immunity, yet microbial pathogens often trigger an excessive response, 'cytokine storm', harmful to the host. Full T-cell activation requires interaction of costimulatory receptors B7-1(CD80) and B7-2(CD86) expressed on antigen-presenting cells with CD28 expressed on the T cells. We created short peptide mimetics of the homodimer interfaces of the B7 and CD28 receptors and examined their ability to attenuate B7/CD28 coligand engagement and signaling through CD28 for inflammatory cytokine induction in human immune cells, and to protect from lethal toxic shock in vivo.
View Article and Find Full Text PDFSkin microbiome dysbiosis and the role of Staphylococcus aureus in atopic dermatitis in adults and children: A narrative review.
J Eur Acad Dermatol Venereol
June 2023
Department Dermatology and Allergy, Ludwig-Maximilian University, Munich, Germany.
A dysfunctional epidermal barrier, which may be associated with mutations in the filaggrin gene in genetically predisposed individuals or harmful effects of environmental agents and allergens, contributes to the development of atopic dermatitis (AD) due to an interplay between the epithelial barrier, immune defence and the cutaneous microbiome. The skin of patients with AD is frequently over-colonized by biofilm-growing Staphylococcus aureus, especially during flares, causing dysbiosis of the cutaneous microbiota and a decrease in bacterial diversity that inversely correlates with AD severity. Specific changes in the skin microbiome can be present before clinical AD onset in infancy.
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