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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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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.

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