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Untitled - D Ank Unlimited

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interfollicular region 398 interleukin-1 receptor (IL1R)<br />

γ is acid-labile and is formed mainly by T lymphocytes<br />

stimulated by antigen or mitogen. This immune interferon<br />

was known as type II in the past. Whereas the ability of<br />

interferon to prevent infection of noninfected cells is species-specific,<br />

it is not virus-specific. Essentially, all viruses<br />

are subject to its inhibitory action. Interferons induce<br />

formation of a second inhibitory protein that prevents viral<br />

messenger RNA translation. In addition to interferon γ<br />

formation by T cells activated with mitogen, natural killer<br />

cells also secrete it. Interferons are not viricidal.<br />

interfollicular region<br />

Tissue separating lymphoid follicles situated in a group; it<br />

exhibits a predominance of mature T cells encircling high<br />

endothelial venules (HEVs).<br />

interleukin (IL)<br />

A general term for numerous cytokines synthesized by leukocytes.<br />

Includes multiple secreted proteins that facilitate<br />

inflammation exchange among leukocytes and activate signaling<br />

that regulates hematopoietic cell growth, differentiation,<br />

and function.<br />

Interleukin-1α.<br />

interleukin-1 (IL1)<br />

The two proteins comprising the IL1 molecule and designated<br />

IL1α and IL1β belong to the interleukin-1 superfamily<br />

of cytokine molecules. The molecules identified within<br />

the IL1 superfamily include IL18 and cytokines encoded<br />

by six more genes with structural homology to IL1α, IL1β,<br />

or IL1RA. These latter six members are terned IL1F5<br />

through IL1F10. IL1α, IL1β, and IL1RA are now known as<br />

IL1F1, IL1F2, and IL1F3. IL33 is an additional member of<br />

the IL1 family; it is also known as IL1F11. Macrophages,<br />

monocytes and dendritic cells synthesize IL1α and IL1β,<br />

which constitute significant parts of the body’s inflammatory<br />

response to infection. These cytokines elevate adhesion<br />

molecule expression on endothelial cells to facilitate<br />

transmigration of leukocytes to sites of infection and reset<br />

the hypothalamus thermoregulatory center, which causes<br />

an elevation in body temperature manifested as fever. Thus,<br />

IL1 is an endogenous pyrogen. IL1 also plays a significant<br />

role in regulation of hematopoiesis. IL1 is a cytokine synthesized<br />

by activated mononuclear phagocytes stimulated<br />

by ribopolysaccharide or by interaction with CD4 + T lymphocytes.<br />

It is a monokine and a mediator of inflammation,<br />

sharing many properties in common with tumor necrosis<br />

factors (TNFs). IL1, IL6, and TNF-α induce a variety<br />

Interleukin-1β.<br />

of inflammatory responses early during infection. IL1 is<br />

composed of two principal polypeptides of 17 kDa, each<br />

with isoelectric points of 5.0 and 7.0. They are designated<br />

IL1α and IL1β, respectively. Genes found on chromosome<br />

2 encode these two molecular species. They have the same<br />

biological activities and bind to the same receptors on cell<br />

surfaces. Both IL1α and IL1β are derived by proteolytic<br />

cleavage of 33-kDa precursor molecules. IL1α acts as a<br />

membrane-associated substance, whereas IL1β is found free<br />

in the circulation. IL1 receptors are present on numerous<br />

cell types. IL1 may activate adenylate cyclase, elevating<br />

cAMP levels and then activating protein kinase A, or it may<br />

induce nuclear factors that serve as cellular gene transcriptional<br />

activators. IL1 may induce synthesis of enzymes<br />

that generate prostaglandins, which may in turn induce<br />

fever, a well known action of IL1. The actions of IL1 differ<br />

according to whether it is produced in lower or higher concentrations.<br />

At low concentrations, the effects are mainly<br />

immunoregulatory. IL1 acts with polyclonal activators to<br />

facilitate CD4 + T lymphocyte proliferation and B lymphocyte<br />

growth and differentiation. It stimulates multiple<br />

cells to act as immune or inflammatory response effector<br />

cells. It also induces further synthesis of itself and of IL6<br />

by mononuclear phagocytes and vascular endothelium. It<br />

resembles TNF in inflammatory properties. IL1 secreted<br />

in greater amounts produces endocrine effects as it courses<br />

through the peripheral blood circulation. For example, it<br />

produces fever and promotes the formation of acute phase<br />

plasma proteins in the liver. It also induces cachexia.<br />

Natural inhibitors of IL1 may be produced by mononuclear<br />

phagocytes activated by immune complexes in humans. The<br />

inhibitor is biologically inactive and prevents the action of<br />

IL1 by binding with its receptor, serving as a competitive<br />

inhibitor. Corticosteroids and prostaglandins suppress IL1<br />

secretion. IL1 was formerly called lymphocyte-activating<br />

factor (LAF).<br />

interleukin-1 receptor (IL1R)<br />

An 80-kDa receptor found on T lymphocytes, chondrocytes,<br />

osteoblasts, and fibroblasts that binds IL1α and<br />

IL1β. Helper/inducer CD4 + T lymphocytes are richer in<br />

IL1R than suppressor/cytotoxic (CD8 + ) T cells. IL1R has

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