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B cell abnormalities in systemic lupus erythematosus.

Amrie C Grammer1, Peter E Lipsky

  • 1Autoimmunity Branch of the Intramural Research Program, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA. grammera@mail.nih.gov

Arthritis Research & Therapy
|June 8, 2004
PubMed
Summary

Systemic lupus erythematosus (SLE) involves pathogenic autoantibodies from plasma cells, with ectopic germinal centers in lupus nephritis kidneys. Genetic factors influence T and B cell responses and clearance of apoptotic material, crucial for understanding SLE pathogenesis.

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Area of Science:

  • Immunology
  • Autoimmunity
  • Genetics

Background:

  • Systemic lupus erythematosus (SLE) is a chronic autoimmune disease.
  • Pathogenic autoantibodies are produced by short- and long-lived plasma cells.
  • Ectopic germinal centers and autoantibody-secreting plasma cells are found in lupus nephritis kidneys.

Purpose of the Study:

  • To review genetic susceptibility loci for SLE.
  • To explore the role of T and B cells in humoral immunity.
  • To highlight the involvement of B lymphocytes in plasma cell differentiation.

Main Methods:

  • Review of candidate genetic susceptibility loci for SLE.
  • Analysis of genes influencing T and B cell activation, proliferation, cytokine/chemokine responsiveness, and apoptosis.

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  • Examination of genes involved in the clearance of apoptotic material and autoantigens.

    • Main Results:

    • Candidate SLE genetic loci affect plasma cell differentiation and survival.
    • Genes influencing T and B cell function in germinal center-derived humoral immunity are implicated.
    • B cell activating factor (BAFF) signaling pathways are critical for plasma cell differentiation.

    Conclusions:

    • Genetic factors play a significant role in SLE pathogenesis by influencing immune cell function and survival.
    • Understanding the intricate B cell signaling pathways is crucial for developing targeted SLE therapies.
    • The clearance of apoptotic material and autoantigens is a key process affected in SLE.