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Blood, 15 May 2001, Vol. 97, No. 10, pp. 2932-2940
CHEMOKINES
Ligation of CD11b and CD11c  2 integrins by
antibodies or soluble CD23 induces macrophage inflammatory protein 1
(MIP-1) and MIP-1 production in primary human monocytes through a
pathway dependent on nuclear factor- B
Roger Rezzonico,
Veronique Imbert,
Rachel Chicheportiche, and
Jean-Michel Dayer
From the Division of Immunology and Allergy, Clinical
Immunology Unit (Hans Wilsdorf Laboratory), Department of Internal
Medicine, University Hospital, Geneva, Switzerland; and INSERM U526,
Faculté de Médecine, Nice, France.
Chemokines and adhesion molecules such as integrins play a major
part in the trafficking, extravasation, and recruitment of leukocytes
to inflammatory sites. This study investigated the effects of
 2 integrin engagement on chemokine production by freshly isolated human monocytes. We found that ligation of CD11b or CD11c but
not CD11a  chains of 2 integrins by antibodies or
soluble CD23 (sCD23) fusion proteins rapidly induced transcription and secretion of interleukin 8, macrophage inflammatory protein (MIP) 1,
and MIP-1. Because the promoters of these chemokine genes contain
 B binding sites, we assessed the possible role of nuclear factor-B (NF-B) in controlling induction of the genes through 2 integrin engagement. Electrophoretic mobility shift
assays showed that sCD23 or antibodies to CD11b or to CD11c
up-regulated DNA-binding activity of NF-B. Activation of NF-B was
accompanied by degradation of its cytosolic inhibitor IB-.
Blockade of depletion of IB- by proteasome inhibitors (proteasome
inhibitor I or acetyl-leucinyl-leucinyl-norleucinal) led to concomitant
inhibition of NF-B DNA-binding activity and expression of MIP-1
and MIP-1 messenger RNA induced by 2 integrin ligation. These results suggest that triggering of CD11b or CD11c 2 integrin on primary human monocytes provides
activation signals leading to nuclear translocation of NF-B and
subsequent secretion of MIP-1 and MIP-1 that may have an
important role in recruitment of other inflammatory cells during
initiation of an inflammatory response.
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