Abstract
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.