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Macrophages induce differentiation of plasma cells through CXCL10/IP-10

Wei Xu1, HyeMee Joo, Sandra Clayton

  • 1Baylor Institute for Immunology Research, Dallas, TX 75204, USA. wei.xu.wx6@roche.com

The Journal of Experimental Medicine
|September 19, 2012
PubMed

Insights

Resident macrophages stimulate B cells to become plasma cells (PCs) via CXCL10/IP-10 and VCAM-1. This interaction is crucial for antibody production and immune response.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Plasma cells (PCs) are essential for antibody production.
  • Resident macrophages (Ms) in tonsils are found near CD138(+) PCs.

Purpose of the Study:

  • To elucidate the role of macrophages in B cell differentiation into plasma cells.
  • To identify the molecular mechanisms underlying this interaction.

Main Methods:

  • Isolation and in vitro generation of human macrophages.
  • Co-culture of macrophages with activated B cells.
  • Analysis of cytokine secretion (e.g., CXCL10/IP-10, IL-6) and cell surface molecule expression (e.g., VCAM-1).
  • Assessment of B cell differentiation into CD138(+)CD38(++) PCs.
  • In vivo studies using IP-10-deficient mice challenged with NP-Ficoll.

Main Results:

  • Human macrophages drive B cell differentiation into CD138(+)CD38(++) PCs.
  • This differentiation is mediated by secreted CXCL10/IP-10 and VCAM-1 contact.
  • Macrophage IP-10 production is induced by B cell-derived IL-6 and STAT3 phosphorylation.
  • IP-10 amplifies IL-6 production by B cells, sustaining STAT3 signaling for PC differentiation.
  • IP-10-deficient mice exhibit reduced NP-specific PCs and lower antibody titers.

Conclusions:

  • Macrophages and B cells engage in a novel dialog regulating plasma cell differentiation.
  • CXCL10/IP-10 acts as a key factor promoting plasma cell differentiation.
  • This macrophage-B cell crosstalk is critical for effective antibody responses.

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