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      Targeting CD22 with the monoclonal antibody epratuzumab modulates human B-cell maturation and cytokine production in response to Toll-like receptor 7 (TLR7) and B-cell receptor (BCR) signaling.

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          Abstract

          Abnormal B-cell activation is implicated in the pathogenesis of autoimmune diseases, including systemic lupus erythematosus (SLE). The B-cell surface molecule CD22, which regulates activation through the B-cell receptor (BCR), is a potential target for inhibiting pathogenic B cells; however, the regulatory functions of CD22 remain poorly understood. In this study, we determined how targeting of CD22 with epratuzumab (Emab), a humanized anti-CD22 IgG1 monoclonal antibody, affects the activation of human B-cell subsets in response to Toll-like receptor 7 (TLR7) and BCR engagement.

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          Autoreactive B cell responses to RNA-related antigens due to TLR7 gene duplication.

          Prapaporn Pisitkun, Jonathan A Deane, Michael J. Difilippantonio … (2006)
          Antibodies against nuclear self-antigens are characteristic of systemic autoimmunity, although mechanisms promoting their generation and selection are unclear. Here, we report that B cells containing the Y-linked autoimmune accelerator (Yaa) locus are intrinsically biased toward nucleolar antigens because of increased expression of TLR7, a single-stranded RNA-binding innate immune receptor. The TLR7 gene is duplicated in Yaa mice because of a 4-Megabase expansion of the pseudoautosomal region. These results reveal high divergence in mouse Y chromosomes and represent a good example of gene copy number qualitatively altering a polygenic disease manifestation.
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            RNA-associated autoantigens activate B cells by combined B cell antigen receptor/Toll-like receptor 7 engagement

            Christina Lau, Courtney Broughton, Abigail S. Tabor … (2005)
            Previous studies (Leadbetter, E.A., I.R. Rifkin, A.H. Hohlbaum, B. Beaudette, M.J. Shlomchik, and A. Marshak-Rothstein. 2002. Nature. 416:603–607; Viglianti, G.A., C.M. Lau, T.M. Hanley, B.A. Miko, M.J. Shlomchik, and A. Marshak-Rothstein. 2003. Immunity. 19:837–847) established the unique capacity of DNA and DNA-associated autoantigens to activate autoreactive B cells via sequential engagement of the B cell antigen receptor (BCR) and Toll-like receptor (TLR) 9. We demonstrate that this two-receptor paradigm can be extended to the BCR/TLR7 activation of autoreactive B cells by RNA and RNA-associated autoantigens. These data implicate TLR recognition of endogenous ligands in the response to both DNA- and RNA-associated autoantigens. Importantly, the response to RNA-associated autoantigens was markedly enhanced by IFN-α, a cytokine strongly linked to disease progression in patients with systemic lupus erythematosus (SLE). As further evidence that TLRs play a key role in autoantibody responses in SLE, we found that autoimmune-prone mice, lacking the TLR adaptor protein MyD88, had markedly reduced chromatin, Sm, and rheumatoid factor autoantibody titers.
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              Germinal centres and B cell lymphomagenesis.

              Katia Basso, Riccardo Dalla-Favera (2015)
              Germinal centres (GCs) are involved in the selection of B cells secreting high-affinity antibodies and are also the origin of most human B cell lymphomas. Recent progress has been made in identifying the functionally relevant stages of the GC and the complex trafficking mechanisms of B cells within the GC. These studies have identified transcription factors and signalling pathways that regulate distinct phases of GC development. Notably, these factors and pathways are hijacked during tumorigenesis, as revealed by analyses of the genetic lesions associated with various types of B cell lymphomas. This Review focuses on recent insights into the mechanisms that regulate GC development and that are relevant for human B cell lymphomagenesis.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Arthritis Res. Ther.
                Title: Arthritis research & therapy
                Publisher: Springer Nature
                ISSN (Electronic): 1478-6362
                ISSN (Print): 1478-6354
                Publication date (Electronic): May 15 2017
                Volume: 19
                Issue: 1
                Affiliations
                [1 ] Division of Rheumatology, Department of Medicine, University of Washington, Seattle, WA, 98109, USA. giltiayn@uw.edu.
                [2 ] Department of Immunology, University of Washington, Seattle, WA, 98109, USA. giltiayn@uw.edu.
                [3 ] Department of Immunology, University of Washington, Seattle, WA, 98109, USA.
                [4 ] UCB Celltech, Slough, UK.
                [5 ] Division of Rheumatology, Department of Medicine, University of Washington, Seattle, WA, 98109, USA.
                Article
                Publisher Item ID: 10.1186/s13075-017-1284-2
                DOI: 10.1186/s13075-017-1284-2
                PMC ID: 5433084
                PubMed ID: 28506291
                SO-VID: 71e1f2b9-6800-4901-be32-0f5110a7ae1a
                History

                Keywords: Antibodies,B cells,B-cell targeted therapy,CD22,Epratuzumab,IL-10,IL-6,Systemic lupus erythematosus,TLR7
                Data availability:
                Keywords: Antibodies, B cells, B-cell targeted therapy, CD22, Epratuzumab, IL-10, IL-6, Systemic lupus erythematosus, TLR7

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