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Generation of Human CD40-activated B cells
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Human CD5 promotes B-cell survival through stimulation of autocrine IL-10 production

Hélène Gary-Gouy1, Julie Harriague, Georges Bismuth

  • 1Laboratoire d'immunologie, Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 543, Paris, France.

Blood
|October 24, 2002
PubMed

Insights

CD5 enhances B-cell survival by promoting interleukin-10 (IL-10) production and dampening B-cell receptor (BCR) signaling. This study reveals CD5

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • CD5 negatively regulates B-cell receptor (BCR) signaling and is upregulated post-BCR stimulation, contributing to B-cell tolerance.
  • CD5 is constitutively expressed on long-lived B-1 cells, which produce interleukin-10 (IL-10) via unknown mechanisms, unlike CD5(-) B-2 cells.

Purpose of the Study:

  • To investigate the relationship between CD5 expression and IL-10 production in B cells.
  • To elucidate the role of CD5 in B-cell survival and BCR signaling.

Main Methods:

  • Analysis of IL-10 production in human peripheral blood CD5(+) and CD5(-) B cells after BCR activation.
  • Introduction of CD5 into CD5(-) B cells to assess its effect on IL-10 production and promoter activity.
  • Evaluation of CD5's impact on B-cell apoptosis and BCR-induced Ca(2+) response.

Main Results:

  • Human peripheral blood CD5(+) B cells exhibit higher IL-10 production than CD5(-) B cells following BCR activation.
  • Transfection of CD5 into CD5(-) B cells induces IL-10 production by activating its promoter and mRNA synthesis, with the cytoplasmic domain being sufficient.
  • CD5 confers protection against apoptosis in normal human B cells post-BCR stimulation and reduces the BCR-induced Ca(2+) response.

Conclusions:

  • CD5 directly promotes IL-10 production in B cells, contributing to their survival.
  • CD5 exerts negative feedback on BCR signaling, mitigating pathways that could lead to cell death.
  • CD5 plays a dual role in B-cell homeostasis: promoting survival via IL-10 and regulating signaling pathways.

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