000			03736nam a22006977a 4500
008			240807s20242024 xxu||||| |||| 00| 0 eng d
022			_a1664-3224
024			_aPMC11061367 [pmc]
040			_aOvid MEDLINE(R)
099			_a38694513
245			_aPrevalence of anti-lymphocyte IgM autoantibodies driving complement activation in COVID-19 patients.
251			_aFrontiers in Immunology. 15:1352330, 2024.
252			_aFront. immunol.. 15:1352330, 2024.
253			_aFrontiers in immunology
260			_c2024
260			_fFY2024
260			_p2024
265			_sepublish
265			_tMEDLINE
266			_d2024-08-07
266			_z2024/05/02 04:06
520			_aDiscussion: IgM ALAb and complement activation against lymphocytes may contribute to the acute lymphopenia observed in COVID-19 patients. Copyright © 2024 Perez-Diez, Liu, Calderon, Bennett, Lisco, Kellog, Galindo, Memoli, Rocco, Epling, Laidlaw, Sneller, Manion, Wortmann, Poon, Kumar and Sereti.
520			_aIntroduction: COVID-19 patients can develop autoantibodies against a variety of secreted and membrane proteins, including some expressed on lymphocytes. However, it is unclear what proportion of patients might develop anti-lymphocyte antibodies (ALAb) and what functional relevance they might have.
520			_aMethods: We evaluated the presence and lytic function of ALAb in the sera of a cohort of 85 COVID-19 patients (68 unvaccinated and 17 vaccinated) assigned to mild (N=63), or moderate/severe disease (N=22) groups. Thirty-seven patients were followed-up after recovery. We also analyzed in vivo complement deposition on COVID-19 patients' lymphocytes and examined its correlation with lymphocyte numbers during acute disease.
520			_aResults: Compared with healthy donors (HD), patients had an increased prevalence of IgM ALAb, which was significantly higher in moderate/severe disease patients and persisted after recovery. Sera from IgM ALAb+ patients exhibited complement-dependent cytotoxicity (CDC) against HD lymphocytes. Complement protein C3b deposition on patients' CD4 T cells was inversely correlated with CD4 T cell numbers. This correlation was stronger in moderate/severe disease patients.
546			_aEnglish
650			_a*Autoantibodies
650			_a*Complement Activation
650			_a*COVID-19
650			_a*Immunoglobulin M
650			_a*SARS-CoV-2
650			_aAdult
650			_aAged
650			_aAutoantibodies/bl [Blood]
650			_aAutoantibodies/im [Immunology]
650			_aCD4-Positive T-Lymphocytes/im [Immunology]
650			_aComplement Activation/im [Immunology]
650			_aComplement C3b/im [Immunology]
650			_aCOVID-19/bl [Blood]
650			_aCOVID-19/im [Immunology]
650			_aFemale
650			_aHumans
650			_aImmunoglobulin M/bl [Blood]
650			_aImmunoglobulin M/im [Immunology]
650			_aLymphocytes/im [Immunology]
650			_aLymphopenia/bl [Blood]
650			_aLymphopenia/im [Immunology]
650			_aMale
650			_aMiddle Aged
650			_aPrevalence
650			_aSARS-CoV-2/im [Immunology]
650			_zAutomated
651			_aMedStar Washington Hospital Center
656			_aMedicine/Infectious Disease
657			_aJournal Article
657			_aResearch Support, Non-U.S. Gov't
700			_aWortmann, Glenn W _bMWHC
790			_aPerez-Diez A, Liu X, Calderon S, Bennett A, Lisco A, Kellog A, Galindo F, Memoli MJ, Rocco JM, Epling BP, Laidlaw E, Sneller MC, Manion M, Wortmann GW, Poon R, Kumar P, Sereti I
856			_uhttps://dx.doi.org/10.3389/fimmu.2024.1352330 _zhttps://dx.doi.org/10.3389/fimmu.2024.1352330
942			_cART _dArticle
999			_c14613 _d14613