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WHICH ANTIVIRAL TREATMENT OPTIONS ARE SUITABLE FOR THERAPY OF PATIENTS INFECTED WITH THE OMIC... Treatment with recombinant monoclonal antibodies (mAbs) that neutralize SARS-CoV-2 can reduce the risk for severe disease. In contrast, neutralization of the Omicron variant is dramatically reduced,1 indicating that immunity following infection by previously circulating SARS-CoV-2 variants provides little to no protection against the Omicron variant. Keywords: antibody; omicron; SARS-CoV-2; spike EN antibody omicron SARS-CoV-2 spike 1 3 3 05/31/22 20220501 NES 220501 The severe acute respiratory syndrome coronavirus 2 Omicron variant (B.1.1.529) swept the globe with breathtaking speed, rapidly displacing the Delta variant and causing record numbers of new infections. [Extracted from the article]

Objective In vitro studies suggest that the type I interferon (IFN) signature seen in most lupus patients results from Fcγ receptor-mediated uptake of nucleic acid-containing immune complexes by plasmacytoid dendritic cells and engagement of endosomal Toll-like receptors. The aim of this study was to reexamine the pathogenesis of the IFN signature in vivo. Methods Lupus was induced in mice by injecting pristane. Some mice were treated with normal immunoglobulin or with cobra venom factor to deplete complement. The IFN signature was evaluated by polymerase chain reaction. The IFN signature also was determined in C4-deficient patients and control subjects. Results Wild-type C57BL/6 mice with pristane-induced lupus developed a strong IFN signature, which was absent in immunoglobulin-deficient (μMT), C3−/−, and CD18−/− mice. Intravenous infusion of normal IgM, but not IgG, restored the IFN signature in μMT mice, and the IFN signature in wild-type mice was inhibited by depleting complement, suggesting that opsonization by IgM and complement is involved in IFN production. Consistent with that possibility, the levels of 'natural' IgM antibodies reactive with dead cells were increased in pristane-treated wild-type mice compared with untreated controls, and in vivo phagocytosis of dead cells was impaired in C3-deficient mice. To examine the clinical relevance of these findings, we identified 10 C4-deficient patients with lupus-like disease and compared them with 152 C4-intact patients and 21 healthy controls. In comparison with C4-intact patients, C4-deficient patients had a different clinical/serologic phenotype and lacked the IFN signature. Conclusion These studies define previously unrecognized roles of natural IgM, complement, and complement receptors in generating the IFN signature in lupus. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a severe autoimmune disorder of unknown etiology. Major autoantigens include immunoglobulin G (which is targeted by rheumatoid factor), citrullinated proteins, and the heterogeneous nuclear ribonucleoprotein (hnRNP) A2. To obtain more insight into the pathogenic role of arthritogenic autoantigens, we studied autoimmune responses in two animal models of RA, which are independent of immunization with exogenous antigens, namely human tumor necrosis factor-α (TNF-α)-transgenic (hTNFtg) mice and rats with pristane-induced arthritis (PIA). Serologic and cellular studies revealed autoantibodies to hnRNP-A2 in these animals and pronounced T-cell reactivity to hnRNP-A2 and the presence of rheumatoid factor in PIA, while citrullinated antigens were not targeted. Furthermore, hnRNP-A2 was found to be highly overexpressed in the joints of mice and rats affected by arthritis. Thus, unspecific proinflammatory stimuli, such as TNF-α or pristane, may induce pathogenic autoimmune reactions that may drive an inflammatory process, leading to the development of erosive arthritis. [ABSTRACT FROM AUTHOR]