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muramyl dipeptide (MDP) 516 myasthenia gravis (MG)<br />

H<br />

HO<br />

O H<br />

H<br />

OH<br />

H<br />

with measles–mumps–rubella virus vaccine before admission<br />

to elementary school.<br />

muramyl dipeptide (MDP)<br />

N-Acetyl-muramyl-l-alanyl-d-isoglutamine; the active<br />

compound responsible for the immunologic adjuvant properties<br />

of complete Freund’s adjuvant. It is an extract of the<br />

peptidoglycans of cell walls of mycobacteria in complete<br />

Freund’s adjuvant that has the immunopotentiating property<br />

of inducing delayed-type hypersensitivity and boosting antibody<br />

responses. It induces fever and lyses blood platelets<br />

and may produce a temporary leukopenia; however, purified<br />

derivatives without adverse side effects have been prepared<br />

for use as immunologic adjuvants and may prove useful for<br />

use in human vaccines.<br />

muromonab CD3 (injection)<br />

A murine monoclonal antibody specific for CD3 antigen of<br />

human T cells used as an immunosuppressant. For intravenous<br />

administration only. It is biochemically purified IgG2a<br />

immunoglobulin that counteracts allograft rejection, possibly<br />

by blocking T cell function that plays a principal role in acute<br />

allograft rejection. It interacts with and inhibits the functioning<br />

of CD3 molecules in human T cell surface membranes<br />

associated with antigen recognition structures of T cells<br />

and is critical for signal transduction. It inhibits all known<br />

Orthoclone<br />

OKT®3<br />

CH 2 OH<br />

O<br />

C<br />

CH 3<br />

H3C CH C NH CH C NH CH C NH2 CH 3<br />

O<br />

O<br />

(CH 2 ) 2<br />

COOH<br />

N-acetylmuramyl-L-alanyl-D-isoglutamine<br />

H<br />

NH<br />

Muramyl dipeptide (MDP).<br />

O<br />

O<br />

Antigen<br />

recognition<br />

structure<br />

CD3 complex<br />

Orthocone OKT®3 blocks T cell effect or function<br />

involved in renal allograft rejection.<br />

T cell<br />

T cell functions and interacts with most peripheral T cells<br />

in blood and body tissues. Following cessation of therapy, T<br />

cell function returns to normal within approximately 1 week.<br />

Within minutes following administration, the number of<br />

circulating CD2 + , CD3 + , CD4 + , and CD8 + T cells decreases<br />

precipitously. T cell activation leads to the release of numerous<br />

cytokines and/or lymphokines believed to be responsible<br />

for many of the acute clinical effects that follow muromonab<br />

CD3 therapy. Antibodies have been detected. The mean time<br />

of appearance of IgG antibodies is 20 days.<br />

mutagen<br />

A chemical, radiation or other agent that can induce a<br />

mutation.<br />

mutant<br />

A mutation in a gene, protein, or cell.<br />

mutation<br />

A structural change in a gene that leads to a sudden and<br />

stable alteration in the genotype of a cell, virus, or organism.<br />

It is a heritable change in the genome of a cell, virus,<br />

or organism apart from that induced through the incorporation<br />

of “foreign” DNA. It represents an alteration in the<br />

base sequence of DNA. Germ cell mutations may be inherited<br />

by future generations, whereas somatic cell mutations<br />

are inherited only by the progeny of cells produced through<br />

mitotic division. A point mutation is an alteration in a single<br />

base pair. Mutations in chromosomes may be expressed as<br />

translocation, deletion, inversion, or duplication.<br />

Nerve<br />

Activation of<br />

muscle<br />

Acetylcholine<br />

Acetylcholine<br />

receptor<br />

Myasthenia gravis (MG).<br />

Nerve<br />

IgG<br />

Activation of<br />

muscle inhibited<br />

myasthenia gravis (MG)<br />

An autoantibody-mediated autoimmune disease. Antibodies<br />

specific for the nicotinic acetylcholine receptor (AChR)<br />

of skeletal muscle react with the postsynaptic membranes<br />

at neuromuscular junctions and diminish the number of<br />

functional receptors. Patients develop muscular weakness<br />

and some voluntary muscle fatigue. The severe muscle<br />

weakness may interfere with breathing if respiratory<br />

muscles are affected. Thus, MG is a receptor disease mediated<br />

by antibodies. The nicotinic AChR is the autoantigen.<br />

Contemporary research hopes to identify epitopes on the<br />

autoantigens that interact with B and T cells in an autoimmune<br />

response. AChR is a four-subunit transmembrane<br />

protein. Most autoantibodies in humans are against the main<br />

immunogenic regions (MIRs). Antibodies against the MIRs<br />

cross link AChR molecules, leading to their internalization<br />

and lysosomal degradation followed by a decreased number<br />

of postsynaptic membrane AChRs. Humans with MG

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