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egional enteritis 616 relapsing polychondritis
regional enteritis
Inflammatory bowel disease characterized by chronic segmental
lymphocytic and granulomatous inflammation of the
gastrointestinal tract.
regulator of complement activation (RCA) cluster
A gene cluster on a 950-kb DNA segment of the long arm of
chromosome 1 that encodes the CR1, CR2, C4bp, and DAF
homologous proteins.
regulators of complement activation (RCAs)
A group of structurally homologous soluble and membrane
proteins that interact with C4 and C3 and inhibit activation
of complement. They include C4bP, decay-accelerating
factor (DAF), membrane cofactor protein (MCP), factors
H and I, CR1 gel caps, CR2 gel caps, vitronectin, clusterin,
MIRL, and HRF. They are comprised of 60 to 70 amino
acid consensus repeat sequences. Also termed complement
control proteins (CCPs).
regulatory CD4 + T cells
CD4 + T cells that are antigen-specific and act as T regulatory
cells by suppressing immune responses.
regulatory peptides (plants)
Generated as a component of local acquired resistance in
plants. They include the ethylene (ET) and jasmonate (JA)
plant hormones that mimic inflammatory mediators in
mammals, as well as salicylic acid.
regulatory T cells
T lymphocytes that inhibit other immune system cell
responses. CD4 + subsets, including T reg, Tr1 and Th3 cells,
and the CD8 + subset. Ts cells comprise this category.
Inhibitory effects demonstrable in vitro are attributable to
intercellular contacts and secretion of immunosuppressive
cytokines. Suppressor T cells are examples of regulatory
T cells.
Reiter complement fixation test (historical)
A diagnostic test for syphilis that used an antigen derived
from a protein extract of Treponema pallidum
Stratum
corneum
Basement
membrane
Chondro-fibrous
junction
Marginal cartilage
Dermal
vessels
Relapsing polychondritis.
(Reiter strain) to identify antibodies formed against
Treponema group antigens.
rejection
An immune response to an organ allograft such as a kidney
transplant. Hyperacute rejection is due to preformed antibodies
and is apparent within minutes following transplantation.
Antibodies reacting with endothelial cells cause
complement to be fixed, which attracts polymorphonuclear
neutrophils and results in denuding of the endothelial
linings of vascular walls. This causes platelets and fibrin
plugs to block blood flow to the transplanted organ, which
becomes cyanotic and must be removed. Only a few drops
of bloody urine are usually produced. Segmental thrombosis,
necrosis, and fibrin thrombi form in the glomerular
tufts, accompanied by hemorrhage in the interstitium and
mesangial cell swelling; IgG, IgM, and C3 may be deposited
in arteriole walls. Acute rejection occurs within days
to weeks following transplantation and is characterized
by extensive cellular infiltration of the interstitium. These
cells are largely mononuclear and include plasma cells,
lymphocytes, immunoblasts, macrophages, and neutrophils.
Tubules become separated, and the tubular epithelium
undergoes necrosis. Endothelial cells are swollen and vacuolated.
Vascular edema, bleeding with inflammation, renal
tubular necrosis, and sclerosed glomeruli occur. Chronic
rejection occurs more than 60 days following transplantation
and may be characterized by structural changes such
as interstitial fibrosis, sclerosed glomeruli, mesangial
proliferative glomerulonephritis, crescent formation, and
other changes.
relapse
The reoccurrence of clinical manifestations of disease in an
individual who was formerly in remission.
relapsing polychondritis
Inflammation of the cartilage, especially that of the
external pinnae of the ears, causing them to lose their
structural integrity. It appears to have an immunological
Fluorescent deposits