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Untitled - D Ank Unlimited

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liver–kidney microsome 1 (LKM-1) autoantibodies 458 long-acting thyroid stimulator (LATS)<br />

antibodies can be shown to interact with hepatocyte and<br />

proximal renal tubule cell cytoplasm. The antibodies are<br />

not demonstrable in the sera of non-A, non-B chronic<br />

active hepatitis patients.<br />

liver–kidney microsome 1 (LKM-1) autoantibodies<br />

Autoantibodies associated with autoimmune hepatitis type<br />

II. Their principal feature is the exclusive staining of the<br />

P3 portions of the proximal renal tubules. Sixty-seven<br />

percent of patients with this disease have antibodies to<br />

liver cytosol type I (anti-LC-1). Cytochrome P-450 2D6<br />

is the major antigen for LKM-1 autoantibodies, which are<br />

specific for cytoplasmic constituents of hepatocytes and<br />

proximal renal tubule cells. They are present in selected<br />

patients with antinuclear antibody (ANA)-negative autoimmune<br />

chronic active hepatitis (CAH) (HBsAg negative).<br />

They are not found in CAH non-A, non-B. LKM-1autoantibody-positive<br />

CAH type II is the most frequent<br />

autoimmune liver disease in children, who have a relatively<br />

poor prognosis. LKM-1 autoantibodies are not believed<br />

to be pathogenic in autoimmune CAH of children. They<br />

show specificity for cytochrome P-450. LKM-2 autoantibodies<br />

are present in tienilic acid (Ticrynafen)-induced<br />

hepatitis. LKM-3 autoantibodies are present in 10% of<br />

chronic delta virus hepatitis cases. The LKM-1 antigen is<br />

cytochrome P-450IID6. The LKM-2 antigen is cytochrome<br />

P-450IIC8/9/10.<br />

liver–kidney microsome 2 (LKM-2) autoantibodies<br />

Antibodies associated only with drug-induced hepatitis<br />

caused by tienilic acid and not an autoimmune hepatitis.<br />

These antibodies are specific for cytochrome P-450-2 C9.<br />

liver–kidney microsome 3 (LKM-3) autoantibodies<br />

An autoantibody that detects a protein band of 55 kDa in<br />

approximately 10% of patients with autoimmune chronic<br />

hepatitis type II.<br />

liver membrane (LM) antibodies<br />

Antibodies specific for the 26-kDa LM protein target antigen<br />

in the sera of 70% of autoimmune chronic active hepatitis<br />

patients who are HBsAg-negative. These antibodies are<br />

demonstrable by immunofluorescence, and they may also<br />

be demonstrated in patients with primary biliary cirrhosis,<br />

chronic hepatitis B, alcoholic liver disease, and sometimes<br />

Sjögren’s syndrome. Lupoid autoimmune chronic active<br />

hepatitis patients may develop antibodies against liver<br />

membrane and also against smooth muscle and nuclear<br />

constituents. Liver membrane antibodies are not useful for<br />

diagnosis or prognosis.<br />

liver membrane autoantibodies<br />

A heterogeneous group of autoantibodies that include<br />

liver-specific membrane lipoprotein (LSMP) autoantibodies<br />

linked to chronic autoimmune hepatitis (AIH). They<br />

lack disease specificity but are useful prognostically for<br />

treatment withdrawal. Characteristic autoantibodies usually<br />

aid in the diagnosis of autoimmune hepatitis. Persistence or<br />

reappearance of liver-specific protein antibodies in chronic<br />

AIH patients in remission during treatment withdrawal may<br />

signify reactivation of the disease.<br />

LM autoantibodies<br />

Antimicrosomal antibodies that react exclusively with liver<br />

tissue have been found in drug-induced hepatitis caused by<br />

dihydralazine. They interact with cytochrome P-450-1A2.<br />

LM antibodies against cytochrome P-450-1A2 in non-druginduced<br />

autoimmune liver disease suggest that the liver<br />

disease may be a manifestation of autoimmune polyendocrine<br />

syndrome type II (APS-1).<br />

LMP-2 and LMP-7<br />

Catalytic subunits of the organelles (proteasomes) that<br />

degrade cytosolic proteins into peptides in the major histocompatibility<br />

complex (MHC) class I pathway of antigen<br />

presentation. MHC genes encode these two subunits that<br />

are upregulated by INF-γ and are especially significant in<br />

the generation of MHC class I-binding peptides.<br />

LMP genes<br />

Two genes located in the major histocompatibility complex<br />

(MHC) class II regions in humans and mice that code for<br />

proteasome subunits. They are closely associated with the<br />

two TAP genes.<br />

L o dose (historical)<br />

The largest amount of toxin that, when mixed with one<br />

unit of antitoxin and injected subcutaneously into a 250-g<br />

guinea pig, produces no toxic reaction.<br />

local acquired resistance<br />

Metabolic changes in plant cells that result in the deposition<br />

or cross linking of lipoproteins and other locally acquired<br />

resistance molecules to strengthen plant cell walls and<br />

isolate a pathogenic microorganism. Antimicrobial peptides<br />

and plant regulatory peptides that activate pathogenesisrelated<br />

proteins are induced.<br />

local anaphylaxis<br />

A relatively common type I immediate hypersensitivity<br />

reaction. Local anaphylaxis is mediated by immunoglobulin<br />

E (IgE) cross linked by allergen molecules at the surfaces<br />

of mast cells that then release histamines and other pharmacological<br />

mediators that produce signs and symptoms.<br />

The reaction occurs in a particular target organ such as the<br />

gastrointestinal tract, skin, or nasal mucosa. Hay fever and<br />

asthma represent examples.<br />

local immunity<br />

Immunologic reactivity confined principally to a particular<br />

anatomic site such as the respiratory or gastrointestinal<br />

tract. Local antibodies and lymphoid cells present in the<br />

area may mediate a specific immunologic effect. For<br />

example, secretory IgA produced in the gut may react to<br />

food or other ingested antigens.<br />

loci<br />

Plural of locus.<br />

locus<br />

The precise location of a gene on a chromosome or other<br />

marker; the DNA at that position. The use of locus is sometimes<br />

restricted to regions of DNA that are expressed.<br />

locus accessibility<br />

The extent to which the chromatin architecture of a specific<br />

antigen receptor gene permits it to be a substrate for the<br />

recombinase complex. Controlled by enhancers.<br />

London forces<br />

Forces that contribute somewhat to the stabilization of<br />

the antigen–antibody complex resulting from attraction of<br />

oscillating dipoles of atoms and molecules moving their<br />

electrons from one side to another. Dispersion forces occur<br />

only when the two molecules are very close together and<br />

decrease with the sixth power of the distance between<br />

interaction groups.<br />

long-acting thyroid stimulator (LATS)<br />

An immunoglobulin G (IgG) autoantibody that mimics<br />

the action of thyroid-stimulating hormone in its effect on

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