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The role of MIP‐1α in Inflammation and hematopoiesis
Author(s) -
Cook Donald N.
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.59.1.61
Subject(s) - biology , proinflammatory cytokine , chemokine , inflammation , macrophage inflammatory protein , haematopoiesis , immunology , cxcl2 , bone marrow , microbiology and biotechnology , stem cell , chemokine receptor
Macrophage inflammatory protein 1α (MIP‐1α) is a member of the C‐C subfamily of chemokines, a large superfamily of low‐molecular‐weight, inducible proteins that exhibit a variety of proinflammatory activities in vitro including leukocyte Chemotaxis. MIP‐1α is a particularly interesting chemokine, because in addition to its proinflammatory activities, it inhibits the proliferation of hematopoietic stem cells in vitro and in vivo. Here, the biologic properties of MIP‐1α are reviewed in light of recent data on mice homozygous for a disruption of the MIP‐1α gene. The MIP‐1α null mice have no overt abnormalities of peripheral blood or bone marrow cells, indicating that MIP‐1α is not necessary for normal hematopoiesis. However, the MIP‐1α null mice have a reduced inflammatory response to influenza virus and are resistant to coxsackievirus‐induced myocarditis. These data demonstrate that MIP‐1α is required for a normal inflammatory response to these viruses. Agents that inhibit the action of MIP‐1α may therefore prove useful for controlling inflammation in these and other settings.