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Untitled - D Ank Unlimited

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parasite immunity 555 parietal cell autoantibodies (PCAs)<br />

parasite immunity<br />

The cytokine network is critical in parasitic infection.<br />

Contemporary research is attempting to untangle this complex<br />

network to develop appropriate mechanisms to combat<br />

infections. Partial success has been achieved in attempting<br />

to control the direction of an immune response by incorporating<br />

cytokines into a vaccine against leishmaniasis.<br />

Interleukin-12 (IL12) has been used to prevent granuloma<br />

formation in schistosomiasis. A fine balance must be<br />

maintained between ensuring protection and reducing the<br />

possibilities of counterprotection. The primary concern in<br />

parasitic infections is not to determine whether an immune<br />

response occurs but whether the interaction between parasite<br />

and host will lead to protection or pathological changes<br />

or a combination. It is necessary to determine which antigens<br />

induce protection, how this protection may be induced<br />

artificially, what causes the pathological changes, and how<br />

they may be countered. No commercially available vaccines<br />

against any human parasitic diseases exist, and only a few<br />

against parasites of veterinary importance are available.<br />

parasites<br />

Organisms that derive sustenance from living hosts such as<br />

worms and protozoa. Eukaryotic organisms with several chromosomes<br />

in a nucleus surrounded by a membrane. Includes<br />

single-celled protozoa and multicellular helminth worms that<br />

range in size from a few micrometers to several meters.<br />

parathyroid hormone autoantibodies<br />

Autoantibodies to parathyroid hormone have been observed<br />

in unexplained hypocalcemia and hypoparathyroidism associated<br />

with normal or increased concentrations of immunoreactive<br />

parathyroid hormone.<br />

paratope<br />

The antigen-binding site of an antibody molecule, the variable<br />

(V) domain, or T cell receptor that binds to an epitope on an<br />

antigen. It is the variable or Fv region of an antibody molecule<br />

and the site for interaction with an epitope of an antigen molecule.<br />

It is complementary for the epitope for which it is specific.<br />

A paratope is the portion of an antibody molecule where<br />

the hypervariable regions are located. There is less than 10%<br />

variability in the light and heavy chain amino acid positions in<br />

the variable regions. There is a 20 to 60% variability in amino<br />

acid sequence in the so-called “hot spots” located at light chain<br />

amino acid positions 29 to 34, 49 to 52, and 91 to 95 and at<br />

heavy chain positions 30 to 34, 51 to 63, 84 to 90, and 101 to<br />

110. Great specificity is associated with this variability and is<br />

the basis of an idiotype. This variability permits recognition of<br />

multiple antigenic determinants.<br />

parenteral<br />

Administration or injection of a substance into the animal<br />

body by any route except the alimentary tract.<br />

parietal cell antibodies<br />

Antibodies present in 50 to 100% of patients with pernicious<br />

anemia (PA) and in 2% of normal individuals. Their<br />

frequency increases with aging and in subjects with insulindependent<br />

diabetes mellitus. The frequency of parietal cell<br />

antibodies diminishes with disease duration in pernicious<br />

anemia. Parietal cell autoantibodies in pernicious anemia<br />

and in autoimmune gastritis recognize the α and β subunits<br />

of the gastric proton pump (H + /K + ATPase) that are the<br />

principal target antigens. Parietal cell antibodies react with<br />

the α and β subunits of the gastric proton pump and inhibit<br />

the acid-producing H + /K + adenosine triphosphatase of the<br />

Pernicious anemia; parietal cell antibody (FITC-labeled).<br />

gastric mucosa. Parietal cell antibodies relate to type A<br />

gastritis, for which fundal mucosal atrophy, achlorhydria,<br />

development of pernicious anemia, and autoimmune endocrine<br />

disease are characteristic.<br />

Gastric parietal cell autoantibody.<br />

Autoantibody: gastric parietal cell + kidney.<br />

parietal cell autoantibodies (PCAs)<br />

Autoantibodies specific for the α and β subunits of the gastric<br />

H + /K + -ATPase (gastric proton pump) that secretes acid into<br />

the stomach lumen and is expressed specifically in gastric<br />

parietal cells. Although parietal cell antibodies can occur in<br />

5% of healthy subjects, they occur in high frequency in pernicious<br />

anemia. They are related to type A gastritis, for which<br />

P

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