We are analyzing https://link.springer.com/article/10.1186/ar3433.

Title:
Mechanisms of B cell autoimmunity in SLE | Arthritis Research & Therapy
Description:
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is known to be associated with polyclonal B-cell hyperreactivity. The underlying causes of the diffuse B-cell over-reactivity are unclear, but potential candidates include (a) intrinsic hyper-reactivity leading to polyclonal B-cell activation with disturbed activation thresholds and ineffective negative selection; (b) lack of immunoregulatory functions; (c) secondary effects of an overactive inflammatory environment, such as overactive germinal center and ectopic follicular activity; and/or (d) disturbed cytokine production by non-B immune cells. These mechanisms are not mutually exclusive and may operate to varying extents and at varying times in SLE. Phenotypic and molecular studies as well as the results of recent clinical trials have begun to provide new insights to address these possibilities. Of importance, new information has made it possible to distinguish between the contribution played by abnormalities in central checkpoints that could lead to a pre-immune repertoire enriched in autoreactive B cells, on the one hand, and the possibility that autoimmunity arises in the periphery from somatic hypermutation and abnormal selection during T cell-dependent B-cell responses on the other. There is an intriguing possibility that apoptotic material bound to the surface of follicular dendritic cells positively selects autoreactive B cells that arise from non-autoreactive B-cell precursors as a result of somatic hypermutation and thereby promotes the peripheral emergence of autoimmunity.
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Keywords {🔍}

cells, pubmed, sle, lupus, article, google, scholar, bcell, cas, systemic, erythematosus, memory, central, cell, patients, autoantibodies, plasma, autoimmunity, activation, blood, autoreactive, autoimmune, somatic, arthritis, disease, selection, activity, hypermutation, human, gcs, peripheral, data, increased, rheum, lipsky, abnormalities, role, immunol, result, subjects, mice, expression, generation, dörner, checkpoints, apoptotic, enhanced, pathogenic, studies, preimmune,

Topics {✒️}

anti-cd20-mediated b-cell depletion steady-state plasmablasts/plasma cells anti-neutrophil cytoplasmic antibody-positive igd-cd27-cd95+ b-cell subset pre-immune b-cell compartment pre-immune b-cell repertoire post-gc b-cell subsets igd-cd27+ post-switched memory pre-immune b-cell populations cell-dependent b-cell responses polyclonal b-cell hyper-reactivity igd-cd27+ post-switched cells pre-defined b-cell subsets cell-dependent b-cell activation short-lived plasmablasts producing pre-immune checkpoints represent long-term belimumab treatment x-linked lymphoproliferative disease cd62l-/β7- plasma cells b-cell hyper-responsiveness polyclonal b-cell hyperreactivity long-lived plasma cell pre-immune repertoire enriched herapeutic b-cell depletion systemic lupus erythematosus-delineation b-cell depletion therapy subsequent b-cell ontogeny pathologic t-cell responses antibody-secreting plasmablasts t-cell antigen recognition diffuse b-cell hyperactivity targeted b-cell therapy exaggerated t-cell responses anti-double-stranded dna restricts nuclear factor-kappa polyclonal b-cell activation intrinsic b-cell defect decreasing b-cell reactivity single-stranded dna/rna genome-wide association scan stringent t-cell control memory b-cell subset cell-independent extrafollicular responses peripheral b-cell subsets late b-cell differentiation regulatory cd19+/cd24high/cd38high ig-producing plasma cells β7 integrin [80] long-lived plasma cells increased b-cell hyperactivity

Questions {❓}

Lee HS, Bae SC: What can we learn from genetic studies of systemic lupus erythematosus?

Schema {🗺️}

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         description:Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is known to be associated with polyclonal B-cell hyperreactivity. The underlying causes of the diffuse B-cell over-reactivity are unclear, but potential candidates include (a) intrinsic hyper-reactivity leading to polyclonal B-cell activation with disturbed activation thresholds and ineffective negative selection; (b) lack of immunoregulatory functions; (c) secondary effects of an overactive inflammatory environment, such as overactive germinal center and ectopic follicular activity; and/or (d) disturbed cytokine production by non-B immune cells. These mechanisms are not mutually exclusive and may operate to varying extents and at varying times in SLE. Phenotypic and molecular studies as well as the results of recent clinical trials have begun to provide new insights to address these possibilities. Of importance, new information has made it possible to distinguish between the contribution played by abnormalities in central checkpoints that could lead to a pre-immune repertoire enriched in autoreactive B cells, on the one hand, and the possibility that autoimmunity arises in the periphery from somatic hypermutation and abnormal selection during T cell-dependent B-cell responses on the other. There is an intriguing possibility that apoptotic material bound to the surface of follicular dendritic cells positively selects autoreactive B cells that arise from non-autoreactive B-cell precursors as a result of somatic hypermutation and thereby promotes the peripheral emergence of autoimmunity.
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      headline:Mechanisms of B cell autoimmunity in SLE
      description:Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is known to be associated with polyclonal B-cell hyperreactivity. The underlying causes of the diffuse B-cell over-reactivity are unclear, but potential candidates include (a) intrinsic hyper-reactivity leading to polyclonal B-cell activation with disturbed activation thresholds and ineffective negative selection; (b) lack of immunoregulatory functions; (c) secondary effects of an overactive inflammatory environment, such as overactive germinal center and ectopic follicular activity; and/or (d) disturbed cytokine production by non-B immune cells. These mechanisms are not mutually exclusive and may operate to varying extents and at varying times in SLE. Phenotypic and molecular studies as well as the results of recent clinical trials have begun to provide new insights to address these possibilities. Of importance, new information has made it possible to distinguish between the contribution played by abnormalities in central checkpoints that could lead to a pre-immune repertoire enriched in autoreactive B cells, on the one hand, and the possibility that autoimmunity arises in the periphery from somatic hypermutation and abnormal selection during T cell-dependent B-cell responses on the other. There is an intriguing possibility that apoptotic material bound to the surface of follicular dendritic cells positively selects autoreactive B cells that arise from non-autoreactive B-cell precursors as a result of somatic hypermutation and thereby promotes the peripheral emergence of autoimmunity.
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