Untitled - D Ank Unlimited

collagen (type I, II, and III) autoantibodies 183 colon antibodies
Fibril
Triple helix
α-Chain
Gly
X
Gly Gly
Y Y
X X
Collagen.
collagen (type I, II, and III) autoantibodies
Autoantibodies found in various autoimmune diseases such
as mixed connective tissue disease (MCTD), systemic lupus
erythematosus (SLE), progressive systemic sclerosis (PSS),
rheumatoid arthritis (RA), and vasculitis. Approximately
85% of SLE patients have antibodies against type I collagen.
Type II collagen autoantibodies in rodents and monkeys have
led to arthritis. Autoantibodies to types I, II, and III collagen
have been identified in adult and juvenile rheumatoid arthritis
and relapsing polychondritis. Individuals with hypersensitivity
reactions to collagen implants may manifest immunity
to native and denatured collagens. Autoantibodies to type
II collagen have been associated with RA and relapsing
polychondritis patients. Autoimmunity to type II collagen has
been hypothesized to have a role in the pathogenesis of RAs.
Autoantibodies to type II collagen have also been reported
in scleroderma and SLE and possibly in inner ear diseases.
Collagen type III antibodies have been found in 44% of SLE
patients and 85% of RA patients.
collagen disease and arthritis panel
A cost-effective battery of tests to diagnose rheumatic
disease that includes the erythrocyte sedimentation rate and
assays for rheumatoid factor (RA test), antinuclear antibody,
uric acid levels, and C-reactive protein.
collagen disease/lupus erythematosus diagnostic panel
A battery of serum tests for the diagnosis of collagen vascular
disease that yields the most information for the least cost.
collagen-induced arthritis (CIA)
The deliberate injection of DBA/1J mice with type II collagen
incorporated into complete Freund’s adjuvant to produce
arthritis in multiple joints as a consequence of autoimmunity.
A murine model of rheumatoid arthritis in humans.
collagen type IV (CIV22)
Anti-collagen type IV is a mouse monoclonal antibody that
detects collagen type IV, the major component of the basal
lamina. Antibodies to this molecule confirm its presence
and reveal the morphological appearance of the structure.
Normal tissue stains with this antibody in a fashion consistent
with the sites of mesenchymal elements and epithelial
basal laminae. Collagen IV can also be useful in the classification
of soft tissue tumors; schwannomas, leiomyomas,
and their well differentiated malignant counterparts
usually immunoreact to this antibody. The vascular nature
of neoplasms, hemangiopericytoma, angiosarcoma, and
epithelioid hemangioendothelioma can be revealed by this
antibody with greater reliability than non-specific stains
such as silver reticulum.
Y
collagen type IV autoantibodies
Autoantibodies against collagen type IV that is present in all
human basement membranes including those of the kidney,
eye, cochlea, lung, placenta, and brain. The triple helical
molecules are composed of two α1 chains and one α2 chain
in a chicken wire-like network. Four other type IV collagen
chains (α3 to α6) form a similar network. Autoantibodies
against type IV collagen occur in progressive systemic
sclerosis, Raynaud’s phenomenon, and scleroderma. Seventy
percent of patients with systemic lupus erythematosus (SLE),
Raynaud’s phenomenon, polyarteritis nodosa, or vasculitides
have collagen type IV autoantobodies. Among patients with
thromboangiitis obliterans (Burger’s disease), 35 to 44%
have autoantibodies against types I and IV collagen. Three
fourths of patients develop cell-mediated immunity to these
two collagens. Autoantibodies to basement membrane and
interstitial collagens play a role in the pathogenesis of scleroderma.
Autoantibodies to type IV collagen are found also in
post-streptococcal glomerulonephritis. Circulating antibodies
specific for the NC1 domain of type IV collagen are present
in Goodpasture’s syndrome and lead to rapidly progressive
glomerulonephritis in these subjects. Most Alport syndrome
patients lack α3, α4, and α5 chains in their glomerular basement
membranes.
collagen vascular diseases
A category of connective tissue diseases in which type III
hypersensitivity mechanisms with immune complex of
deposition play a major role. These diseases are characterized
by inflammation and fibrinoid necrosis in tissues.
Patients may manifest involvement of multiple systems,
including the vasculature, joints, skin, kidneys, and other
tissues. These are classic, systemic autoimmune diseases
in most cases. The prototype of this category is systemic
lupus erythematosus (SLE). Other disorders included in this
category are dermatomyositis, polyarteritis nodosa, progressive
systemic sclerosis (scleroderma), rheumatoid arthritis,
and mixed connective tissue disease. They are treated with
immunosuppressive drugs, especially corticosteroids.
collectin receptor
The receptor of C1q, a subcomponent of the complement
component C1.
collectins
A family of structurally related calcium-dependent proteins
or sections with collagen-like domains that bind sugars such
as mannose-binding protein. Collectins may bind to C1q,
thereby activating the complement system, and participate
in innate immunity through their actions as microbial
recognition receptors. These soluble pattern recognition
molecules remove pathogenic microorganisms by opsonization,
agglutination, or the lectin pathway of complement
activation. Examples include mannose-binding lectin and
lung surfactant proteins A and D.
colocalization
Mechanism of differential redistribution of membrane components
into patches and caps used to investigate possible
interactions between various plasma membrane components
or between cell membranes and cytoplasmic structures.
colon antibodies
Immunoglobulin G (IgG) antibodies in the blood sera of 71%
of ulcerative colitis patients may be shown by flow cytometry
to react with rat colon epithelial cells. Antibodies reactive with
a 40-kDa constituent of normal colon extracts have been found
C