26.07.2013 Views

Untitled - D Ank Unlimited

Untitled - D Ank Unlimited

Untitled - D Ank Unlimited

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

immune exclusion 357 immune–neuroendocrine axis<br />

% Injected I*HSA in Total Blood Volume<br />

Equilibration<br />

100<br />

10<br />

1<br />

2<br />

4<br />

Catabolic decay<br />

complexes that have already fixed complement. This is<br />

followed by removal of immune complexes through the<br />

phagocytic actions of mononuclear phagocytes. Immune<br />

elimination also describes an assay to evaluate the antibody<br />

response by monitoring the rate at which a radiolabeled<br />

antigen is eliminated in an animal with specific (homologous)<br />

antibodies in the circulation.<br />

immune exclusion<br />

Prevention of antigen entry into the body by the products of<br />

a specific immune response, such as the blocking of access<br />

by an antigen to the body by mucosal surfaces when secretory<br />

IgA specific for the antigen is present.<br />

immune globulin, human (intravenous, IVEEGAM EN)<br />

Indicated for replacement therapy in individuals with<br />

primary immunodeficiency syndromes including congenital<br />

agammaglobulinemia, common variable immunodeficiency,<br />

X-linked agammaglobulinemia (with or without hyper IgM)<br />

and Wiskott–Aldrich syndrome. Patients with severe combined<br />

immunodeficiency have an impairment of antibody<br />

synthesis and T cell defects. Thus, they may benefit from<br />

replacement therapy with immune globulin even though<br />

the therapy does not correct their basic cellular defects.<br />

Immune globulin IV (human) is very effective in providing<br />

high levels of circulating antibodies within a short time<br />

when intramuscular injections are contraindicated. It has<br />

also been used for Kawasaki syndrome and has other unlabeled<br />

uses including post-transfusion purpura, Guillain-<br />

Barré syndrome, and chronic inflammatory demyelinating<br />

polyneuropathy. It is also useful in treatment of selected<br />

autoimmune diseases such as rhesus hemolytic disease,<br />

factor VIII deficiencies, bullous pemphigoid, rheumatoid<br />

arthritis, Sjögren’s syndrome, type I diabetes mellitus, IgG4<br />

subclass deficiencies, intractable epilepsy (possibly caused<br />

by IgG2 subclass deficiency), cystic fibrosis, trauma, thermal<br />

injury (e.g., severe burns), cytomegalovirus infection,<br />

neuromuscular disorders, prophylaxis of infections associated<br />

with bone marrow transplantation, and GI protection<br />

(i.e., oral administration).<br />

6<br />

8<br />

10<br />

Days after Injection of I*HSA<br />

Immune elimination.<br />

Immune<br />

elimination<br />

12<br />

14<br />

immune hemolysis<br />

The lysis of erythrocytes through the action of specific<br />

antibody and complement.<br />

immune inflammation<br />

Reaction to injury mediated by an adaptive immune<br />

response to antigen. Neutrophils and macrophages responding<br />

to T cell cytokines may comprise the inflammatory cellular<br />

infiltrate.<br />

immune interferon<br />

Synonym for interferon-γ.<br />

immune modulation<br />

Refer to immunomodulation.<br />

immune modulator<br />

An agent that alters the level of an immune response.<br />

immune network hypothesis of Jerne<br />

The antigen-binding sites (paratopes) of antibody molecules<br />

are encoded by variable region genes and have idiotopes as<br />

phenotypic markers. Each paratope recognizes idiotopes on<br />

a different antibody molecule. Interaction of idiotypes with<br />

anti-idiotypes is physiologic idiotypy and is shared among<br />

immunoglobulin (Ig) classes. This comprises antibodies<br />

produced in response to the same antigen. The idiotypic<br />

network consists of the interaction of idiotypes involving<br />

free molecules as well as B and T lymphocyte receptors.<br />

Idiotypes are considered central in immunoregulation<br />

involving autoantigens.<br />

immune–neuroendocrine axis<br />

A bidirectional regulatory circuit exists between the<br />

immune and neuroendocrine systems that affect each<br />

other. Receptors for neurally active polypeptides, neurotransmitters,<br />

and hormones are present on immune<br />

system cells, whereas receptors reactive with products of<br />

the immune system may be identified on nervous system<br />

cells. Neuroendocrine hormones have variable immunoregulatory<br />

effects mediated through specific receptors.<br />

Neurotransmitter influence on cell function is determined in<br />

part by the receptor-linked signal amplification associated<br />

with second messenger systems. Neuroimmunoregulation<br />

is mediated either through a neural pathway involving pituitary<br />

peptides and adrenal steroid hormones or through a<br />

second pathway consisting of direct innervation of immune<br />

system tissues. The thymus, spleen, bone marrow, and<br />

perhaps other lymphoid organs contain afferent and efferent<br />

nerve fibers. Adrenocorticotrophic hormone (ACTH),<br />

endorphins, enkephalins, and adrenal cortical steroids<br />

derived from the pituitary represent one direction for modulating<br />

the immune response. For example, prolactin (PRL)<br />

regulates lymphocyte function. Stimulated lymphocytes or<br />

nonstimulated macrophages may produce neuroendocrine<br />

hormone-related peptides, ACTH, and endorphins. The participation<br />

of these substances in a stress response represents<br />

the opposite direction of regulation. Thymic hormones may<br />

also induce an endocrine response. Neuroendocrine hormones<br />

may exert a positive or negative regulatory effect on<br />

macrophages that play a key role in both inflammation and<br />

immune responsiveness. Leukocyte mediators are known to<br />

alter both central nervous system and immune system functions.<br />

Interleukin-1 (IL1) acts on the hypothalamus to produce<br />

fever and participates in antigen-induced activation.<br />

IL1 is synthesized by macrophages and plays a major role in<br />

inflammation and immune responsiveness. Substance P (SP)<br />

has been postulated to have an effect in hypersensitivity<br />

I

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!