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membrane cofactor of proteolysis (MCP or CD46) 488 membranous glomerulonephritis
and 2, and factor H and C4-binding protein in plasma. MCP
is also called CD46.
membrane cofactor of proteolysis (MCP or CD46)
A host cell membrane protein that functions in association
with factor I to cleave C3b to its inactive derivative iC3b,
thereby blocking formation of convertase.
membrane complement receptors
Receptors are expressed on blood cells and tissue macrophages
of humans. They include Clq-R (Clq receptor),
CR1 (C3b/C4b receptor; CD35), CR2 (C3d/Epstein–Barr
virus [EBV] receptor; CD21), CR3 (iC3b receptor; CD11b/
CD18), CR4 (C3bi receptor; CD11c/CD18), CR5 (C3dg-dimer
receptor), fH-R (factor H receptor), C5a-R (C5a receptor),
and C3a/C4a–R (C3a/C4a receptor). Ligands for C receptors
generated by the classic or alternate pathway include fluid
phase activation peptides of C3, C4, and C5 designated C3a,
C4a, and C5a that are anaphylatoxins that interact with C3a/
C4a–R or C5a–R and participate in inflammation. Other
ligands for C receptors include soluble or particulate complement
proteins deposited on immune complexes. Fixed C4
and C3 fragments (C4b, C3b, C3bi, C3dg, and C3d), Clq, and
a factor H constitute these ligands. These receptors play a
major role in facilitating improved recognition of pathogenic
substances. They aid the elimination of bacteria and soluble
immune complexes. Neutrophils, monocytes, and macrophages
express C3 receptors on their surface. Neutrophils
and erythrocytes express immune adherence receptors
(CR1s) on their surfaces. Four other receptors for C3 are designated
CR2, CR3, CR4, and CR5. Additional receptors for
complement components other than C3 and C3a are termed
Clq receptor, C5a-R (C5a receptor), C3a-R (C3a receptor),
and fH-R (factor H receptor).
membrane immunofluorescence
The reaction of a fluorochrome-labeled antibody with surface
receptors of viable cells. This reaction of fluorescent
antibody with surface antigens rather than internal antigens
is the basis for many immunologic assays such as labeling
of lymphocytes with such reagents for immunophenotyping
by flow cytometry, patching, and capping and to detect
changes in surface antigens through antigenic variation.
Cytoplasm
mlg
Ig-α
Ig-β
Membrane immunoglobulin.
membrane immunoglobulin
Cell surface immunoglobulin that serves as an antigen receptor.
Virgin B cells contain surface membrane IgM and IgD
molecules. Following activation by antigen, the B cells differentiate
into plasma cells that secrete IgM molecules. Whereas
membrane-bound IgM is a four-polypeptide chain monomer,
the secreted IgM is a pentameric molecule containing five
four-chain unit monomers and one J chain. Other immunoglobulin
classes have membrane and secreted types. IgG and
IgA membrane immunoglobulins probably serve as memory
B cell antigen receptors. The segment of the immunoglobulin
introduced into the cell membrane is a hydrophobic
heavy chain region in the vicinity of the carboxyl terminus.
Within a particular isotype, the heavy chain is of greater
length in the membrane form than in the secreted molecule.
This greater length is at the carboxyl terminal end of the
membrane form. Separate mRNA molecules from one gene
encode the membrane and secreted forms of heavy chain.
membrane nibbling
Process whereby a dendritic cell acquires part of the membrane
of an intact living whole cell.
membranoproliferative glomerulonephritis (MPGN)
A nephropathy in which the glomerular basement membrane
is altered and glomerular cells proliferate, especially
in mesangial areas, leading to the synonymous
mesangiocapillary GN. Patients may present with hematuria
and/or proteinuria. In type I MPGN, IgG-, Clq-,
C4-, and C3-containing subendothelial electron-dense
deposits are present in approximately 66% of cases, as
revealed by immunofluorescence and electron microscopy.
Conventional light microscopy reveals splitting of basement
membranes. In type II MPGN, also called dense deposit
disease, the lamina densa of the glomerular basement
membrane appears as an electron-dense ribbon, on either
side of which C3 can be detected by immunofluorescence.
Complement is fixed only by the alternate pathway. Type
II patients have C3 nephritic factor (C3NeF) in their sera
which facilitates stabilization of alternate C3 convertase,
thereby promoting C3 degradation and hypocomplementemia.
Half of these patients develop chronic renal failure
over a 10-year period.
Types of glomerulonephritis.
membranous glomerulonephritis
A disease induced by deposition of electron-dense, immune
(Ag–Ab) deposits in the glomerular basement membrane in
a subepithelial location. This leads to progressive thickening
of glomerular membranes. Most cases are idiopathic,
but membranous glomerulonephritis may follow development
of other diseases such as systemic lupus erythematosus
(SLE), lung or colon carcinoma, and exposure to
gold, mercury, penicillamine, or captopril. It can also be a
sequela of certain infections (e.g., hepatitis B) or metabolic