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leukoagglutinin 447 leukocyte common antigen (LCA, CD45)<br />

leukoagglutinin<br />

An antibody or other substance that induces the aggregation<br />

or agglutination of white blood cells into clumps.<br />

leukocidin<br />

A cytolytic bacterial toxin produced especially by staphylococci.<br />

It is toxic principally for polymorphonuclear leukocytes<br />

and to a lesser extent for monocytes. It contains F and<br />

S components that combine with cell membranes, causing<br />

altered permeability. Less than toxic doses interfere with<br />

locomotion of polymorphonuclear neutrophils (PMNs).<br />

leukocyte<br />

White blood cell. The principal types of leukocytes in the<br />

peripheral blood of humans include polymorphonuclear<br />

neutrophils, eosinophils and basophils (granulocytes), and<br />

lymphocytes and monocytes.<br />

leukocyte activation<br />

The first step in activation is adhesion through surface<br />

receptors on cells. Stimulus recognition is also mediated<br />

through membrane-bound receptors. An inducible<br />

endothelial–leukocyte adhesion molecule that provides<br />

a mechanism for leukocyte–vessel wall adhesion has<br />

been described. Surface-adherent leukocytes undergo<br />

a large prolonged respiratory burst. NADPH oxidase,<br />

which utilizes hexose monophosphate shunt-generated<br />

NADPH, catalyzes the respiratory burst. Both Ca 2+ and<br />

protein kinase C play key roles in the activation pathway.<br />

Complement receptor 3 (CR3) facilitates the ability<br />

of phagocytes to bind and ingest opsonized particles.<br />

Molecules found to be powerful stimulators of polymorphonuclear<br />

neutrophil (PMN) activity include recombinant<br />

interferon-γ (IFN-γ), granulocyte–macrophage<br />

colony-stimulating factor (GM-CSF), tumor necrosis<br />

factor (TNF), and lymphotoxin.<br />

leukocyte adhesion deficiency (LAD)<br />

Recurrent bacteremia with staphylococci or Pseudomonas<br />

linked to defects in the leukocyte adhesion molecules<br />

known as integrins, which mainly alters the ability of leukocytes<br />

to reach extracellular pathogens at sites of infection,<br />

thereby preventing their effective eradication. These<br />

include the CD11/CD18 family of molecules. CD18 β<br />

chain gene mutations lead to a lack of complement receptors<br />

CR3 and CR4 to produce a congenital disease marked<br />

by recurring pyogenic infections. Deficiency of p150,95,<br />

leukocyte-function-associated antigen 1 (LFA-1), and<br />

complement receptor 3 (CR3) membrane proteins leads to<br />

diminished adhesion properties and mobility of phagocytes<br />

and lymphocytes. All three of these molecules share<br />

a flaw in the synthesis of the 95-kDa β chain subunit.<br />

The defect in mobility is manifested as altered chemotaxis,<br />

defective random migration, and faulty spreading.<br />

Particles coated with C3 are not phagocytized and<br />

therefore fail to activate a respiratory burst. The CR3 and<br />

p150,95 deficiencies account for the defective phagocytic<br />

activity. The T cells of patients with LAD fail to respond<br />

normally to antigen or mitogen stimulation and are also<br />

unable to provide helper function for B cells producing<br />

immunoglobulin. They are ineffective in fatally injuring<br />

target cells, and they do not produce the lymphokine<br />

interferon-γ (IFN-γ). LFA-1 deficiency accounts for the<br />

defective responses of these T lymphocytes and all natural<br />

killer (NK) cells that also have impaired ability to fatally<br />

injure target cells. Clinically, the principal manifestations<br />

are consequences of defective phagocyte function rather<br />

than of defective T lymphocyte function. Patients may<br />

have recurrent severe infections, defective inflammatory<br />

responses, abscesses, gingivitis, and periodontitis. LAD<br />

has two forms; those with the severe deficiency do not<br />

express the three α and four β chain complexes, whereas<br />

those with moderate deficiency express 2.5 to 6% of these<br />

complexes. The two human LAD syndromes thus far<br />

recognized include LAD I, in which the integrin family is<br />

defective, and LAD II, in which sialyl Lewis X , the ligand<br />

for selectins, is absent. LAD has an autosomal-recessive<br />

mode of inheritance; LAD I is attributable to mutations<br />

in the gene that encodes the CD18 protein which is part<br />

of the β 2 integrins, whereas mutations in the gene that<br />

encodes an enzyme needed for the synthesis of leukocyte<br />

ligands for endothelial selectins causes LAD II.<br />

leukocyte adhesion molecule-1<br />

A homing protein found on membranes that combines with<br />

target-cell-specific glycoconjugates. It helps regulate migration<br />

of leukocytes through lymphocytes binding to high<br />

endothelial venules and neutrophil adherence to endothelium<br />

at inflammatory sites.<br />

leukocyte adhesion molecules (LAMs)<br />

Facilitators of vascular endothelium aggregation, chemotaxis,<br />

cytotoxicity, binding of iC3b-coated particles,<br />

lymphocyte proliferation, and phagocytosis. The three<br />

main families of LAMs include the selectins, integrins, and<br />

immunoglobulin superfamily. Leukocyte adhesion deficiencies<br />

are partial or complete inherited deficiencies of cell<br />

surface expression of CD18 and CD11a–c. These deficiencies<br />

prevent granulocytes from migrating to extravascular<br />

sites of inflammation, leading to recurrent infections and<br />

possibly death.<br />

leukocyte adhesion protein<br />

A membrane-associated dimeric glycoprotein composed of<br />

a unique α subunit and a shared 95-kDa β subunit involved<br />

in cell-to-cell interactions. This protein group includes<br />

lymphocyte function-associated antigen 1 (LFA-1) found on<br />

lymphocytes, neutrophils, and monocytes; membrane attack<br />

complex 1 (MAC-1) found on neutrophils, eosinophils,<br />

natural killer (NK) cells, and monocytes; and p150,95,<br />

which is common to all leukocytes.<br />

leukocyte chemotaxis inhibitors<br />

Humoral factors that inhibit the chemotaxis of leukocytes.<br />

They play a role in the regulation of inflammatory<br />

responses of both immune and nonimmune origin.<br />

leukocyte common antigen (LCA, CD45)<br />

A family of high molecular weight glycoproteins (180 to<br />

220 kDa) densely expressed on lymphoid and myeloid cells,<br />

including lymphocytes, monocytes, and granulocytes.<br />

Expression of LCA on leukocytes but not on other cells<br />

makes LCA a valuable marker in immunophenotyping<br />

of tumors to determine histogenetic origin. LCA antigen<br />

function is unknown, but it has a high carbohydrate content<br />

and is believed to be associated with the cytoskeleton. LCA<br />

molecules are heterogeneous and appear on T and B lymphocytes<br />

and selected other hematopoietic cells. Some LCA<br />

epitopes are present in all LCA molecules, while others<br />

are confined to B lymphocyte LCA; still other epitopes are<br />

associated with B cell, CD8 + T cell, and most CD4 + T cell<br />

LCA molecules. About 30 exons are present in the gene that<br />

encodes LCA molecules; it is designated as CD45.<br />

L

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