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Rabbit Anti-Monocyte Chemotactic Protein-1 (MCP-1) Polyclonal antibody, Unconjugated

RRID:AB_90984

Antibody ID

AB_90984

Target Antigen

Monocyte Chemotactic Protein-1 (MCP-1) rat

Proper Citation

(Millipore Cat# AB1834P, RRID:AB_90984)

Clonality

polyclonal antibody

Reference

PMID:24920622

Comments

seller recommendations: ELISA; Western Blot; ELISA, Western Blotting

Host Organism

rabbit

Vendor

Millipore

Cat Num

AB1834P

Publications that use this research resource

Conditional ablation of astroglial CCL2 suppresses CNS accumulation of M1 macrophages and preserves axons in mice with MOG peptide EAE.

  • Moreno M
  • J. Neurosci.
  • 2014 Jun 11

Literature context:


Abstract:

Current multiple sclerosis (MS) therapies only partially prevent chronically worsening neurological deficits, which are largely attributable to progressive loss of CNS axons. Prior studies of experimental autoimmune encephalomyelitis (EAE) induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG peptide), a model of MS, documented continued axon loss for months after acute CNS inflammatory infiltrates had subsided, and massive astroglial induction of CCL2 (MCP-1), a chemokine for CCR2(+) monocytes. We now report that conditional deletion of astroglial CCL2 significantly decreases CNS accumulation of classically activated (M1) monocyte-derived macrophages and microglial expression of M1 markers during the initial CNS inflammatory phase of MOG peptide EAE, reduces the acute and long-term severity of clinical deficits and slows the progression of spinal cord axon loss. In addition, lack of astroglial-derived CCL2 results in increased accumulation of Th17 cells within the CNS in these mice, but also in greater confinement of CD4(+) lymphocytes to CNS perivascular spaces. These findings suggest that therapies designed to inhibit astroglial CCL2-driven trafficking of monocyte-derived macrophages to the CNS during acute MS exacerbations have the potential to significantly reduce CNS axon loss and slow progression of neurological deficits.