This locus represents a small inducible cytokine. The encoded protein, also known as macrophage inflammatory protein 1 alpha, plays a role in inflammatory responses through binding to the receptors CCR1, CCR4 and CCR5. Polymorphisms at this locus may be associated with both resistance and susceptibility to infection by human immunodeficiency virus type 1.[provided by RefSeq, Sep 2010]
OMIM-Description for CCL3/Mip1a
Macrophage inflammatory protein-1 is a so-called monokine that is involved in the acute inflammatory state in the recruitment and activation of polymorphonuclear leukocytes (Wolpe et al., 1988). Sherry et al. (1988) demonstrated 2 protein components of MIP1, called by them alpha and beta.
Chemokine (C-C motif) ligand 3 (CCL3) is a protein that in humans is encoded by the CCL3 gene. CCL3, also known as Macrophage inflammatory protein-1α (MIP-1α), is a cytokine belonging to the CC chemokine family that is involved in the acute inflammatory state in the recruitment and activation of polymorphonuclear leukocytes (Wolpe et al., 1988). Sherry et al. (1988) demonstrated 2 protein components of MIP1, called by them alpha and beta.[supplied by OMIM]
CCL3 is monokine with inflammatory and chemokinetic properties. CCL3 binds to CCR1, CCR4 and CCR5. CCL3 is one of the major HIV-suppressive factors produced by CD8+ T-cells. Recombinant MIP-1-alpha induces a dose-dependent inhibition of different strains of HIV-1, HIV-2, and simian immunodeficiency virus (SIV).
CCL3 is monocyte, chemoattractant, activated T cell and dendritic cell
CCL3 is involved in cytoskeletal regulation
CCL3 is one of the major HIV-suppressive factors produced by CD8+ T cells
CCL3 plays a role as an important mediator of virus-induced inflammation
CCL3 plays a role in eosinophil recruitment in inflammatory states such as occurs in the asthmatic lung
CCL3 inhibits stem cell proliferation
CCL3 contributes to intracellular signaling and other chemokine receptor function
CCL3/CCR1 axis may have a role in the spread of tumoral cells to the lymph nodes and also in the local host defense against the tumor
with CCL4, CCL3 may directly or indirectly affect neuronal excitability, and are implicated in the etiology and pathogenesis of temporal lobe epilepsy
CCL3's expression not only reduces viral pathogenicity but also enhances immunogenicity by recruiting dendritic cells and B cells to the site of immunization, the lymph nodes, and the blood