B cell activation leads to shedding of complement receptor type II (CR2/CD21)

Madhan Masilamani, Daniela Kassahn, Stefan Mikkat, Michael O. Glocker, Harald Illges

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


Complement receptor type II (CR2/CD21) is the major receptor for C3d fragments on immune complexes. CD21 also serves as the receptor for Epstein-Barr virus in humans. On mature B cells, CD21 reduces the threshold of BCR signaling together with CD81, Leu13 and CD19, but it also occurs on other cells of the immune system where it performs unknown functions. A soluble form of CD21 (sCD21) is shed from the cell surface and is found in human blood plasma. An as-yet-unknown protease is thought to be responsible for this shedding. Altered levels of sCD21 occur in plasma in certain clinical conditions. We show here by mass spectrometry that sCD21 in human plasma of healthy donors is predominantly a short form of CD21 without the exon-11-encoded sequences. Whereas the N terminus of sCD21 was found unmodified, the C terminus is truncated, implying that only the extracellular portion of CD21 is shed. Peripheral blood B cells, but not T cells, contribute to the plasma CD21-pool. CD21 shedding is induced by stimulation with PMA plus Ca2+ ionophore, or by stimulation of the BCR with anti-IgM+anti-CD40.

Original languageEnglish
Pages (from-to)2391-2397
Number of pages7
JournalEuropean Journal of Immunology
Issue number9
StatePublished - 1 Sep 2003
Externally publishedYes


  • Mass spectrometry
  • Protease inhibitors
  • Shedding
  • Soluble CD21


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