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Follicular dendritic cells control engulfment of apoptotic bodies by secreting Mfge8

Jan Kranich1, Nike Julia Krautler, Ernst Heinen

  • 1Institute of Neuropathology, University Hospital of Zurich, 8091 Zurich, Switzerland.

The Journal of Experimental Medicine
|May 21, 2008
PubMed

Insights

Follicular dendritic cells (FDCs) provide milk fat globule epidermal growth factor 8 (Mfge8) to macrophages, aiding the removal of apoptotic B cells. FDC dysfunction contributes to autoimmunity by impairing this crucial process.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Milk fat globule epidermal growth factor 8 (Mfge8) is a secreted protein crucial for clearing apoptotic germinal center B cells by tingible-body macrophages (TBMphis).
  • Dysfunction in apoptotic cell clearance is linked to the development of autoimmune diseases.

Purpose of the Study:

  • To investigate the source of Mfge8 in the spleen and its role in TBMphi-mediated clearance of apoptotic B cells.
  • To elucidate the relationship between follicular dendritic cells (FDCs) and Mfge8 in the context of autoimmunity.

Main Methods:

  • Utilized bone-marrow chimeras between wild-type and Mfge8-deficient mice.
  • Analyzed Mfge8 expression in TBMphis under various conditions, including co-culture with Mfge8-expressing stroma and exposure to exogenous Mfge8.
  • Examined lymphotoxin-deficient mice lacking FDCs.

Main Results:

  • Mfge8 in the spleen was primarily derived from FDCs, not TBMphis.
  • Mfge8-deficient TBMphis could acquire Mfge8 when in proximity to Mfge8-expressing stromal cells or in lymph nodes receiving exogenous Mfge8.
  • Lymphotoxin-deficient mice, lacking FDCs, exhibited reduced splenic Mfge8 and developed autoimmunity.

Conclusions:

  • FDCs play a licensing role, providing Mfge8 essential for TBMphi-mediated clearance of apoptotic B cells.
  • FDC malfunction, leading to impaired Mfge8 availability, is implicated in the pathogenesis of autoimmunity.

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