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Literature DB >> 27730250

Developing connections amongst B lymphocytes and deregulated pathways in autoimmunity.

Abstract

Immunologists have long investigated B lymphocytes as solely antibody producing cells. With further studies, it became clear that B cells are able to exert a variety of functions within the immune system, and beyond. As a result, B cells are considered promising targets for immunotherapy in a variety of disorders. Recently, experts in B cell biology and autoimmunity convened to discuss important stepping stones to decipher the complexity of B lymphocyte-mediated pathways in autoimmune diseases.

Entities: Disease

Keywords: atherosclerosis; autoimmune disease; lupus; multiple sclerosis; plasma cell; rheumatoid arthritis

Year: 2016 PMID： 27730250 PMCID： PMC5135078 DOI： 10.2119/molmed.2016.00206

Source DB: PubMed Journal: Mol Med ISSN： 1076-1551 Impact factor: 6.354

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References

36 in total

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Journal: Proc Natl Acad Sci U S A Date: 2016-06-20 Impact factor: 11.205

Developing connections amongst B lymphocytes and deregulated pathways in autoimmunity.

1. B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers.

2. Development of a recombinant immunotoxin for the immunotherapy of autoreactive lymphocytes expressing MOG-specific BCRs.

3. Distinct oligoclonal band antibodies in multiple sclerosis recognize ubiquitous self-proteins.

4. The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus erythematosus.

5. IgG subclass distribution of autoantibodies to DNA and to nuclear ribonucleoproteins in autoimmune diseases.

6. Sustained improvement in rheumatoid arthritis following a protocol designed to deplete B lymphocytes.

Review 7. PTEN: The down side of PI 3-kinase signalling.

8. Transcription factor ABF-1 suppresses plasma cell differentiation but facilitates memory B cell formation.

Review 9. Hallmarks of Tissue-Resident Lymphocytes.

10. IFN-γ receptor and STAT1 signaling in B cells are central to spontaneous germinal center formation and autoimmunity.