{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T11:04:13Z","timestamp":1784113453284,"version":"3.55.0"},"posted":{"date-parts":[[2026,7,11]]},"group-title":"Immunology","reference-count":72,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,7,11]],"date-time":"2026-07-11T00:00:00Z","timestamp":1783728000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"crossref","award":["U19 AI110483"],"award-info":[{"award-number":["U19 AI110483"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,7,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Autoimmune diseases, such as systemic lupus erythematosus (SLE), are underscored by dysregulated B cell function including the production of autoantibodies, skewed population ratios, and aberrant signaling. Given that the family of nuclear factor kappa B (NF-\u03baB) transcription factors govern responses to stimuli, survival, differentiation, and so forth understanding the intricate regulatory network of NF-\u03baB in B cell biology is paramount for unraveling treatments for B cell-linked autoimmune diseases. Here, we focus on a negative regulator of NF-\u03baB signaling, A20 (\n                  <jats:italic>TNFAIP3<\/jats:italic>\n                  ), that deactivates NF-\u03baB transcription factor translocation through the ubiquitination and deubiquitination of target proteins. Haploinsufficiency in A20 results in an autoimmune phenotype and mutations to A20 have been associated with SLE, suggesting implications to B cell function. To investigate the role of A20 in NF-\u03baB in human B cells, we generated a\n                  <jats:italic>TNFAIP3<\/jats:italic>\n                  knockout (KO) Raji cell line. Cells were stimulated with either anti-IgM or Resiquimod (R848) to activate distinct NF-\u03baB signaling pathways. Using qRT-PCR, western blotting, and flow cytometry, we assessed differences in gene expression, protein production, and NF-\u03baB activation. We observed key limitations in using Epstein-Barr virus transformed B cell lines to model inducible NF-\u03baB signaling.\n                <\/jats:p>","DOI":"10.64898\/2026.07.07.737082","type":"posted-content","created":{"date-parts":[[2026,7,12]],"date-time":"2026-07-12T16:10:18Z","timestamp":1783872618000},"source":"Crossref","is-referenced-by-count":0,"title":["Limitations of EBV transformed human Raji B cells as a model for measuring canonical NF-\u03baB activation"],"prefix":"10.64898","author":[{"given":"Rachel","family":"Kidwell","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7716-8504","authenticated-orcid":false,"given":"Christopher D.","family":"Scharer","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, 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