EVO-STIK Plumber's Mait, Non-Setting Putty for Sanitary Joints, Waterproof, 750g

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Barathan, M. et al. Peripheral loss of CD8 + CD161 ++ TCRVα7·2 + mucosal-associated invariant T cells in chronic hepatitis C virus-infected patients. Eur. J. Clin. Invest. 46, 170–180 (2016). Lee, C.H. et al. C/EBPδ drives interactions between human MAIT cells and endothelial cells that are important for extravasation. eLife 7, (2018). Voillet, V. et al. Human MAIT cells exit peripheral tissues and recirculate via lymph in steady state conditions. JCI Insight 3, e98487 (2018). Seach, N. et al. Double-positive thymocytes select mucosal-associated invariant T cells. J. Immunol. 191, 6002–6009 (2013). Provine NM, Klenerman P (April 2020). "MAIT Cells in Health and Disease". Annual Review of Immunology. 38 (1): 203–228. doi: 10.1146/annurev-immunol-080719-015428. PMID 31986071. S2CID 210934618.

Wilgenburg, B. V. et al. MAIT cells contribute to protection against lethal influenza infection in vivo. Nat. Commun. 9, 4706 (2018). Meierovics, A., Yankelevich, W. J. & Cowley, S. C. MAIT cells are critical for optimal mucosal immune responses during in vivo pulmonary bacterial infection. Proc. Natl Acad. Sci. USA 110, E3119–E3128 (2013). In healthy cells, MR1 is sparsely exhibited on the cell surface. However, MR1 expression is upregulated on the surface after cell infection or the introduction of a bacterially-produced MR1 ligand. [7] Once expressed on the surface, MR1, with its antigen ligand covalently-attached, binds to the appropriate MAIT cell TCR. [6] Microbial and viral response [ edit ]Koay, H. F. et al. Diverse MR1-restricted T cells in mice and humans. Nat. Commun. 10, 2243 (2019). The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Publisher’s Note Meermeier, E. W. et al. Human TRAV1-2-negative MR1-restricted T cells detect S. pyogenes and alternatives to MAIT riboflavin-based antigens. Nat. Commun. 7, 12506 (2016). Lepore M, Kalinichenko A, Colone A, Paleja B, Singhal A, Tschumi A, etal. (May 2014). "Parallel T-cell cloning and deep sequencing of human MAIT cells reveal stable oligoclonal TCRβ repertoire". Nature Communications. 5: 3866. Bibcode: 2014NatCo...5.3866L. doi: 10.1038/ncomms4866. PMID 24832684.

Tastan, C. et al. Tuning of human MAIT cell activation by commensal bacteria species and MR1-dependent T-cell presentation. Mucosal Immunol. 11, 1591–1605 (2018). Tony's presentation at the BAPCO Satellite Series event in Newcastle in November 2019 is attached below – and finally as we come into 2022 and beyond there is traction to have MAIT rolled out more widely in the UK. There is now supplier choice – with the AVR Group and ATOS both making their MAIT solutions available via G-Cloud 12 on the Government’s Digital Marketplace; further suppliers are also looking at how they too can support MAIT. Cho, Y. N. et al. Mucosal-associated invariant T cell deficiency in systemic lupus erythematosus. J. Immunol. 193, 3891–3901 (2014). Turtle, C. J., Swanson, H. M., Fujii, N., Estey, E. H. & Riddell, S. R. A distinct subset of self-renewing human memory CD8 + T cells survives cytotoxic chemotherapy. Immunity 31, 834–844 (2009). MAIT cells can be activated by two pathways as follows: via TCR signalling (MR1 dependent) or cytokine signalling alone (MR1 independent). Riboflavin derivatives presented by MR1 of antigen presenting cells (APCs) activate MAIT cells, while the folic acid product is a competitive inhibitor ( 31). Because riboflavin synthesis is broadly conserved among bacteria and fungi, MAIT cells respond to a diverse array of microbes, including known commensals ( 32, 33). Following MR1-mediated activation, MAIT cells rapidly produce a wide range of cytokines, including interferon (IFN)-γ, tumor necrosis factor (TNF), IL-17 and IL-22. These cytokines, either directly (IFN-γ, TNF and IL-17) or indirectly through cell proliferation (IL-22), promote cytolysis of the infected cells, thereby leading to the control of various infections ( 15, 32, 34, 35). MAIT cells can also be activated by inflammatory cytokines alone, such as IL-7, IL-12, IL-18, IL-15 and IFN-α/β, in a TCR-independent manner ( 19, 36, 37). MAIT cells are activated with no known antigens, for instance, during viral infections or sterile auto-immunities. Cytokine-dependent activation of MAIT cells leads to secretion of IFN-γ, TNF and granzyme B, which exert cytotoxic functions ( 36, 37). Transcriptomic analysis of E. coli- and TCR-activated MAIT cells has shown distinct transcriptional reprogramming, including altered pathways, transcription factors and effector molecules, which has been validated by proteomics and metabolomics ( 38). In E. coli -activated MAIT cells, the TWIST1 transcription factor has been identified as a key driver, showing high connectivity to cytokine and chemokine expression ( 38). MAIT Cells in Rheumatic Diseases

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a b Boehm U, Klamp T, Groot M, Howard JC (1997-01-01). "Cellular responses to interferon-gamma". Annual Review of Immunology. 15: 749–795. doi: 10.1146/annurev.immunol.15.1.749. PMID 9143706. Harms, R. Z. et al. Abnormal T cell frequencies, including cytomegalovirus-associated expansions, distinguish seroconverted subjects at risk for type 1 diabetes. Front. Immunol. 9, 2332 (2018). Sundström, P. et al. Human mucosa-associated invariant T cells accumulate in colon adenocarcinomas but produce reduced amounts of IFN-γ. J. Immunol. 195, 3472–3481 (2015). Patel, O. et al. Recognition of vitamin B metabolites by mucosal-associated invariant T cells. Nat. Commun. 4, 2142 (2013).