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M component 484 Medawar, Peter Brian (1915–1987)
M component
A spike or defined peak observed on electrophoresis of
serum proteins which suggests monoclonal proliferation
of mature B lymphocytes synthesizing immunoglobulin
G (IgG), IgA, or IgM. M component can be seen in such
diseases as multiple myeloma, heavy chain disease, and
Waldenström’s macroglobulinemia.
MCP-1 (monocyte chemoattractant protein 1)
A prototypic chemokine of the β (CC) family that was
first isolated as a product of the immediate early gene,
JE, induced by PDGF. Cloning of the human homolog of
JE reveals an encoded protein identical to an authentic
chemokine MCP-1, which is believed to be one of the most
significant chemokines in chronic inflammatory diseases
controlled by mononuclear leukocytes. Tissue sources
include fibroblasts, monocytes, macrophages, mouse spleen
lymphocytes, and endothelial cells, among others. Target
cells include monocytes, hematopoietic precursors, T lymphocytes,
basophils, eosinophils, mast cells, natural killer
(NK) cells, and dendritic cells.
MCP-1 in atherosclerosis
Chemokines are involved in the pathogenesis of atherosclerosis
by promoting directed migration of inflammatory
cells. Monocyte chemoattractant protein-1 (MCP-1), a CC
chemokine, has been detected in atherosclerotic lesions by
anti-MCP-1 antibody detection and in situ hybridization.
MCP-1 mRNA expression has been found in endothelial
cells, macrophages and vascular smooth muscle cells in
atherosclerotic arteries of patients undergoing bypass revascularization.
MCP-1 functions in the development of atherosclerosis
by recruiting monocytes into the subendothelial
cell layer. MCP-1 is critical for the initiation and development
of atherosclerotic lesions. During the progression of
atherosclerosis, low density lipoprotein (LDL) accumulates
within macrophages and monocytes present in the intimal
layer. Deposition of lipids within these cells leads to the formation
and eventual enlargement of atherosclerotic lesions.
Studies suggest a noncholesterol-mediated effect of MCP-1
in the development of atherosclerotic lesions. MCP-1 plays
a crucial role in initiating atherosclerosis by recruiting
macrophages and monocytes to vessel walls.
MCP-2 (monocyte chemoattractant protein 2)
A chemokine of the β (CC) family. It is a variant of MCP-1,
but is independent and has several distinct biological properties
that include eosinophil and basophil activation. The
principal differences between MCP-1 and MCP-2 appear
in the N terminal molecular region. Tissue sources include
fibroblasts, peripheral blood mononuclear cells, leteal cells,
and osteosarcoma cell line MG 63. Target cells include
T lymphocytes, monocytes, eosinophils, basophils, and
natural killer (NK) cells.
MCP-3 (monocyte chemoattractant protein 3)
A chemokine of the β (CC) family that has very different
binding characteristics and actions from MCP-1. MCP-3
binds to unique monocyte receptors shared by MCP-1. In
contrast to MCP-1, MCP-3 is chemotactic to eosinophils and
more potent toward basophils. It is the only β chemokine
that fails to form dimers at elevated concentrations. Tissue
sources include fibroblasts, platelets, mast cells, monocytes,
and osteosarcoma MG-63. Target cells include monocytes,
T cells, basophils, eosinophils, activated natural killer (NK)
cells, dendritic cells, and neutrophils.
M-CSF (macrophage colony-stimulating factor)
Facilitates growth, differentiation, and survival and serves
as an activating mechanism for macrophages and their
precursors. It is derived from numerous sources such as
lymphocytes, monocytes, endothelial cells, fibroblasts,
epithelial cells, osteoblasts, and myoblasts. X-ray crystallography
of recombinant CSF reveals a structure in which
four α helices are placed end to end in two bundles. Human
and mouse M-CSF share 82% homology in the N terminal
227 amino acids of the mature sequence, but there is only
47% homology in the remainder of the molecular structure.
M-CSF derived from humans and from mice has been previously
termed colony-stimulating factor 1 (CSF-1).
MCTD
Acronym for mixed-connective tissue disease.
MDP
Muramyl dipeptide.
measles vaccine
An attenuated virus vaccine administered as a single injection
to children at 2 years of age or between 1 and 10 years
old. Contraindications include a history of allergy or convulsions.
Puppies may be protected against canine distemper
in the neonatal period by the administration of attenuated
measles virus which represents a heterologous vaccine.
Passive immunity from the mother precludes early immunization
of puppies with live canine distemper vaccine.
measles virus vaccine (live, injection)
Measles, a common childhood disease, is induced by a
paramyxovirus. It can be associated with serious complications,
including pneumonia, encephalitis, and even death.
Subjects first vaccinated with measles virus vaccine at 12
months of age or older require revaccination with measles,
mumps, and rubella virus vaccine (live) before entering
elementary school. Revaccination may induce seroconversion.
The Advisory Committee on Immunization Practices
advises that the first dose of measles–mumps–rubella vaccine
be administered at 12 to 15 months of age and that the
second dose be given at 4 to 6 years of age.
measles–mumps–rubella virus vaccine (live, injection)
For simultaneous vaccination in individuals at least 12
months of age. These subjects should be revaccinated prior
to admission to elementary school. Vaccination of persons
exposed to natural measles may afford protection if the vaccine
is administered within 72 hours of exposure. If given a
few days prior to exposure, greater protection is possible.
mechanical barrier
The papilloma virus and a few other infection agents may
penetrate the skin but most microorganisms are excluded
by it. Free fatty acids from sebaceous glands and lactic acid
present in perspiration together with an acid pH of 5 to 6
and the dryness of the skin are unfavorable to microorganisms.
Staphylococcus aureus may colonize hair follicles
and sweat glands to produce furuncles, carbuncles, and
abscesses. Pseudomonas aeruginosa may infect skin
injured by burns. Injury to the gastric mucosa by irradiation
or cytotoxic drugs may culminate in infection by the
normal flora of the intestine.
Medawar, Peter Brian (1915–1987)
British transplantation biologist. Earned a PhD in 1935
at Oxford, where he served as a lecturer in zoology. He
later became a professor of zoology at Birmingham (1947)
and at University College, London (1951). He was named