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10.1016/j.coi.2021.07.011 http://scihub22266oqcxt.onion/10.1016/j.coi.2021.07.011 34418591!8578378!34418591     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Opin+Immunol 2021 ; 72 (ä): 286-297 Nephropedia Template TP {{tp|p=34418591|t=2021. Infections in the monogenic autoimmune syndrome APECED |pdf=|usr=}}{{34418591}} gab.com Text Infections in the monogenic autoimmune syndrome APECED JO: Curr Opin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34418591 #FOAvip Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is caused by mutations in the Autoimmune Regulator (AIRE) gene, which impair the thymic negative selection of self-reactive T-cells and underlie the development of autoimmunity that targets multiple endocrine and non-endocrine tissues. Beyond autoimmunity, APECED features heightened susceptibility to certain specific infections, which is mediated by anti-cytokine autoantibodies and/or T-cell driven autoimmune tissue injury. These include the 'signature' APECED infection chronic mucocutaneous candidiasis (CMC), but also life-threatening coronavirus disease 2019 (COVID-19) pneumonia, bronchiectasis-associated bacterial pneumonia, and sepsis by encapsulated bacteria. Here we discuss the expanding understanding of the immunological mechanisms that contribute to infection susceptibility in this prototypic syndrome of impaired central tolerance, which provide the foundation for devising improved diagnostic and therapeutic strategies for affected patients. Twit Text FOAVip Infections in the monogenic autoimmune syndrome APECED ????Curr Opin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34418591 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34418591 #FOAvip English Wikipedia <ref>{{Cite pmid|34418591}}</ref> Infections in the monogenic autoimmune syndrome APECED #MMPMID34418591 Oikonomou V; Break TJ; Gaffen SL; Moutsopoulos NM; Lionakis MS Curr Opin Immunol 2021[Oct]; 72 (ä): 286-297 PMID34418591show ga Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is caused by mutations in the Autoimmune Regulator (AIRE) gene, which impair the thymic negative selection of self-reactive T-cells and underlie the development of autoimmunity that targets multiple endocrine and non-endocrine tissues. Beyond autoimmunity, APECED features heightened susceptibility to certain specific infections, which is mediated by anti-cytokine autoantibodies and/or T-cell driven autoimmune tissue injury. These include the 'signature' APECED infection chronic mucocutaneous candidiasis (CMC), but also life-threatening coronavirus disease 2019 (COVID-19) pneumonia, bronchiectasis-associated bacterial pneumonia, and sepsis by encapsulated bacteria. Here we discuss the expanding understanding of the immunological mechanisms that contribute to infection susceptibility in this prototypic syndrome of impaired central tolerance, which provide the foundation for devising improved diagnostic and therapeutic strategies for affected patients. |AIRE Protein[MESH] |Animals[MESH] |Autoimmunity[MESH] |Bronchiectasis[MESH] |COVID-19/epidemiology/genetics/*immunology[MESH] |Candidiasis, Cutaneous/epidemiology/genetics/*immunology[MESH] |Clonal Selection, Antigen-Mediated/genetics[MESH] |Disease Susceptibility[MESH] |Humans[MESH] |Immune Tolerance/genetics[MESH] |Polyendocrinopathies, Autoimmune/epidemiology/genetics/*immunology[MESH] |T-Lymphocytes/*immunology[MESH]Infections in the monogenic autoimmune syndrome APECED (epmc).pdf DeepDyve Pubget Overpricing