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Prepublished online as a Blood First Edition Paper on August 8, 2002; DOI 10.1182/blood-2002-05-1525.
Submitted May 24, 2002
Accepted July 17, 2002
Human CD5 promotes B cell survival through stimulation of autocrine IL-10 production
Helene Gary-Gouy, Julie Harriague, Georges Bismuth, Cornelia Platzer, Christian Schmitt, and Ali H Dalloul*
Laboratoire d'Immunologie, INSERM Unite 543, Paris, France
Institut Cochin, INSERM Unite 567, Paris, France
Institute of Anatomy, Friedrisch Sciller University, Iena, Germany
* Corresponding author; email: dalloul{at}ccr.jussieu.fr.
CD5 is a negative regulator of B-cell receptor (BCR) signaling, upregulated after BCR stimulation, and likely contributing to B cell tolerance in vivo. However, CD5 is constitutively expressed on the B-1 subset of B cells. contrary to CD5- B-2 cells, B-1 B cells are long lived due to an autocrine IL-10 production through unknown mechanisms. We demonstrate herein a direct relationship between CD5 expression and IL-10 production. Human periphezral blood CD5+ B cells produce much more IL-10 than CD5- B cells after BCR activation. Introducing CD5 into CD5- B cells induces the production of IL-10 by activating its promoter and the synthesis of its mRNA. The cytoplasmic domain of CD5 is sufficient for this process. CD5 also protects normal human B cells from apoptosis after BCR stimulation while reducing BCR-induced Ca2+ response. We conclude that CD5 supports the survival of B cells by stimulating IL-10 production and by exerting concurrently a negative feedback on BCR-induced signaling events that can promote cell death.
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