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Cloning and characterization of exodus, a novel beta-chemokine
R Hromas, PW Gray, D Chantry, R Godiska, M Krathwohl, K Fife, GI Bell, J Takeda, S Aronica, M Gordon, S Cooper, HE Broxmeyer and MJ Klemsz
Department of Hematology/Oncology and the Walther Oncology Center, Indiana
University Medical Center, Indianapolis 46202, USA.
Chemokines are a family of related proteins that regulate leukocyte
infiltration into inflamed tissue. Some chemokines such as MIP-1 alpha also
inhibit hematopoietic progenitor cell proliferation. Recently, three
chemokines, MIP-1 alpha, MIP-1 beta, and RANTES, have been found to
significantly decrease human immunodeficiency virus production from
infected T cells. We report here the cloning and characterization of a
novel human chemokine termed Exodus for its chemotactic properties. This
novel chemokine is distantly related to other chemokines (28% homology with
MIP-1 alpha) and shares several biological activities. Exodus is expressed
preferentially in lymphocytes and monocytes, and its expression is markedly
upregulated by mediators of inflammation such as tumor necrosis factor or
lipopolysaccharide. Purified synthetic Exodus was found to inhibit
proliferation of myeloid progenitors in colony formation assays. Exodus
also stimulated chemotaxis of peripheral blood mononuclear cells. The
sequence homology, expression, and biological activity indicate that Exodus
represents a novel divergent beta-chemokine.
Volume 89,
Issue 9,
pp. 3315-3322,
05/01/1997
Copyright © 1997 by The American Society of Hematology
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