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Prepublished online as a Blood First Edition Paper on August 8, 2002; DOI 10.1182/blood-2002-05-1525.

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2002-05-1525v1
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Blood, 15 December 2002, Vol. 100, No. 13, pp. 4537-4543

IMMUNOBIOLOGY

Human CD5 promotes B-cell survival through stimulation of autocrine IL-10 production

Hélène Gary-Gouy, Julie Harriague, Georges Bismuth, Cornelia Platzer, Christian Schmitt, and Ali H. Dalloul

From the Laboratoire d'immunologie, Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 543, Paris, France; Département de Biologie Cellulaire, Institut Cochin, INSERM Unité 567, Université Paris V, France; and Institute of Anatomy II, Friedrich Schiller University, Iena, Germany.

CD5 is a negative regulator of B-cell receptor (BCR) signaling that is up-regulated after BCR stimulation and likely contributes to B-cell tolerance in vivo. However, CD5 is constitutively expressed on the B-1 subset of B cells. Contrary to CD5- B-2 B cells, B-1 B cells are long-lived because of autocrine interleukin-10 (IL-10) production through unknown mechanisms. We demonstrate herein a direct relationship between CD5 expression and IL-10 production. Human peripheral blood CD5+ B cells produce 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 the BCR-induced Ca2+ response. We conclude that CD5 supports the survival of B cells by stimulating IL-10 production and by concurrently exerting negative feedback on BCR-induced signaling events that can promote cell death.

© 2002 by The American Society of Hematology.
 

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