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Untitled - D Ank Unlimited

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primary follicle 592 primary structure<br />

patients manifest high titers of antimitochondrial antibodies.<br />

IgM in the serum is elevated. Lymphocytic infiltration and<br />

intrahepatic bile duct destruction occur. Alkaline phosphatase<br />

is greatly increased, in addition to the elevation of<br />

IgM and antimitochondrial antibodies. The M2 antimitochondrial<br />

antibody is most frequently associated with PBC.<br />

In addition to hepatosplenomegaly and skin hyperpigmentation,<br />

patients may develop severe jaundice, petechiae, and<br />

purpura as the disease progresses. Liver transplantation is the<br />

only treatment for end-stage disease.<br />

primary follicle<br />

A densely packed accumulation of resting mature B<br />

lymphocytes and macrophages in a network of follicular<br />

dendritic cells from secondary lymphoid tissues such as the<br />

lymph node cortex or the splenic white pulp, where resting<br />

unstimulated B cells develop into germinal centers when<br />

stimulated by antigen.<br />

primary granule<br />

Azurophil granule.<br />

Antibody Titer<br />

= Anti-A<br />

= Anti-B<br />

Antigen A<br />

Primary<br />

Anti-A response<br />

Antigen A<br />

+<br />

Antigen B<br />

0 2 4 6<br />

Time in Weeks<br />

Primary immune response.<br />

Secondary<br />

Anti-A response<br />

Primary<br />

Anti-B response<br />

8 10 12<br />

primary immune response<br />

The body’s adaptive immune response to first contact with<br />

antigen. It is characterized by a lag period of a few days<br />

following antigen administration before antibodies or specific<br />

T lymphocytes are detectable. The antibody produced<br />

consists mostly of IgM and is of relatively low titer and<br />

low affinity. This is in contrast to the secondary immune<br />

response, in which the latent period is relatively brief and<br />

IgG is the predominant antibody. The most important component<br />

of the primary response is the activation of memory<br />

cells that recognize antigen immediately on second encounter<br />

with antigen, leading to a secondary response. A similar<br />

pattern is followed in cell-mediated responses.<br />

primary immunodeficiency<br />

Diminished immune reactivity attributable to an intrinsic<br />

abnormality of T or B lymphocytes. Development failure<br />

of a segment of the immune system as a consequence of an<br />

inborn genetic mutation.<br />

primary interaction<br />

Antigen and antibody binding that may or may not lead to<br />

a secondary visible reaction such as precipitation. Primary<br />

antigen–antibody interaction may be measured by equilibrium<br />

dialysis, the Farr assay, fluorescence polarization,<br />

fluorescence quenching, and selected radioimmunoassays<br />

such as radioimmunoelectrophoresis.<br />

primary lymphoid follicles<br />

B cell regions, comprised of resting B lymphocytes, of secondary<br />

lymphoid tissues unstimulated by an immune response.<br />

primary lymphoid organ<br />

The site of maturation of B or T lymphocytes. The primary<br />

lymphoid organ for B lymphocytes is the bursa of Fabricius<br />

in avian species and the bone marrow in adult mammals.<br />

By contrast, T cell development occurs in the thymus of<br />

all vertebrates. Stem cell maturation in primary lymphoid<br />

organs occurs without stimulation by antigen.<br />

primary lymphoid tissues<br />

Bone marrow and thymus, the sites of lymphoid development.<br />

primary lysosome<br />

A lysosome that has not yet fused with a phagosome.<br />

primary nodule<br />

Refer to primary follicle.<br />

primary reaction<br />

The actual binding of antibody, via its Fab or antigenbinding<br />

fragment, to its homologous antigen to form an<br />

antibody–antigen complex. After initial contact, the union<br />

of the two substances takes place almost instantaneously<br />

(within milliseconds).<br />

primary response<br />

First response to an immunogen to which the recipient has<br />

not been previously exposed. Both B and T lymphocytes<br />

are activated by epitopes to proliferate and differentiate into<br />

antigen-effector lymphocytes and memory cells. It is principally<br />

an IgM response and generates immunologic memory.<br />

primary sclerosing cholangitis (PSC)<br />

A possible autoimmune liver disease characterized by<br />

inflammation of the large intra- and extrahepatic bile ducts<br />

that eventually leads to strictures and dilatations. The bile<br />

ducts eventually become stenotic and small intrahepatic<br />

bile ducts disappear. Although its etiology is unknown,<br />

chronic portal bacteremia, toxic bile acids, chronic viral<br />

infections, ischemic vascular injury, and immunoregulatory<br />

disorders have been implicated. Antineutrophil cytoplasmic<br />

antibodies (ANCAs) and antinuclear antibodies<br />

(ANAs) are principal features of PSC. Of lesser importance<br />

are anticolon epithelial autoantibodies. Incidence<br />

is predominantly male, in contrast to most autoimmune<br />

diseases. Lymphocytes infiltrate and destroy bile ducts.<br />

Hypergammaglobulinanemia, circulatory immune complexes,<br />

increased metabolism of complement component<br />

C3, and classical pathway activation of complement occur.<br />

Primary structure.<br />

primary structure<br />

The linear amino acid sequence of a polypeptide or<br />

protein molecule.

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