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Nijmegen breakage syndrome (NBS) 533 NOD proteins<br />

reduce NBT. The ability to reduce NBT to the insoluble<br />

formazan crystals depends on the generation of superoxide<br />

in the neutrophil tested.<br />

Nijmegen breakage syndrome (NBS)<br />

A primary immunodeficiency including variable hypogammaglobulinemia<br />

and CID. Ionizing radiation of patient cells<br />

reveals significant levels of chromosomal defects. Induced<br />

by mutations in the gene that encodes nibrin, a protein associated<br />

with the NHEJ pathway of DNA repair.<br />

NK1.1<br />

A natural killer (NK) cell alloantigen identified in selected<br />

inbred mouse strains such as C57BL/6 mice.<br />

NK1.1 CD4 T cells<br />

A minor T cell subset that expresses the NK1.1 marker, a<br />

molecule usually present on natural killer cells. NK1.1 T<br />

lymphocytes also express α:β T cell receptors of limited<br />

diversity and coreceptor molecule CD4 or no coreceptor.<br />

They are present in abundance in the liver and synthesize<br />

cytokines soon after stimulation.<br />

NK1-T cell<br />

A lymphocyte that shares certain characteristics with<br />

T cells such as T cell receptors in addition to those of natural<br />

killer cells.<br />

NK activatory receptors<br />

ITAM-bearing receptors which, when engaged with inhibitory<br />

receptor interaction, lead to natural cytotoxicity and<br />

cytotoxic cytokine secretion by NK cells causing deaths of<br />

target cells bereft of self MHC class I molecules. The group<br />

includes NCR, KAR, NKG2D, -C and –E and Ly-49D, -H,<br />

-P and –W.<br />

NK cell lectin-like receptors<br />

One of the two principal structural classes of NK cell activating<br />

and inhibitory receptors.<br />

NK cells<br />

Refer to natural killer cells.<br />

NK inhibitory receptors<br />

ITIM-bearing receptors that, when engaged by self-MHC<br />

class I molecules on a target, dampen the effects of NK<br />

activatory receptor engagement, thereby inhibiting destruction<br />

of target cells. Includes KIRs; Ly-49A, -B, -C, -E, -F,<br />

-G, Ly-49I: NKG2A and –B; and IL-T2.<br />

NK/T precursor<br />

Common lymphoid progenitor derived predecessor capable<br />

of differentiating into T or NK cells but not B cells.<br />

NKT<br />

Refer to natural killer T cells.<br />

NKT cell<br />

A lymphoid cell that is intermediate between T lymphocytes<br />

and natural killer (NK) cells with respect to morphology<br />

and granule content. Lymphoid cells may be CD4 – 8 – or<br />

CD4 + 8 – weakly expressed α:β T cell receptors (TCRs)<br />

with an invariant α chain and highly restricted β chain<br />

specificity. They have a powerful capacity to synthesize<br />

interleukin-4 (IL4). Many of these TCRs recognize antigens<br />

presented by the nonclassical major histocompatibility<br />

complex (MHC)-like CD1 molecule. Their surface NK1.1<br />

receptors are lectin-like and are believed to recognize<br />

microbial carbohydrates.<br />

NK tolerance<br />

Fostered during NK cell development through selection<br />

of only NK clones bearing NK inhibitory receptors that<br />

are capable of recognizing self-MHC and sending a strong<br />

enough signal to overcome NK activatory receptory signaling<br />

induced by host cells.<br />

N-linked oligosaccharide<br />

An oligosaccharide covalently linked to asparagine<br />

residues in protein molecules. N-linked oligosaccharide<br />

manifests a branched core structure composed of two<br />

N-acetylglucosamine residues and three mannose residues.<br />

The three types differ on the basis of their exterior<br />

branches: (1) high-mannose oligosaccharide reveals two to<br />

six additional mannose residues linked to the polysaccharide<br />

core; (2) complex oligosaccharide composed of two to<br />

five terminal branches that consist of N-acetylglucosamine,<br />

galactose, often N-acetylneuraminic acid, and occasionally<br />

fucose or another sugar; and (3) hybrid molecules<br />

that reveal characteristics of high mannose and complex<br />

oligosaccharides.<br />

N nucleotides<br />

Nontemplated nucleotides that terminal deoxynucleotidyl<br />

transferase (TdT) adds to the 3′ cut ends of V, D, and J<br />

coding segments during rearrangement. They are added<br />

to junctions between V, D, and J gene segments in immunoglobulin<br />

or T cell receptor genes during lymphocyte<br />

development. When as many as 20 of these nucleotides<br />

are added, the diversity of the antibody and T cell receptor<br />

repertoires is expanded.<br />

Nocardia immunity<br />

Infection by microorganisms of this genus usually begins<br />

as a pulmonary infection that may be localized or disseminated.<br />

Nocardia species have complex antigenic structures.<br />

Immunocompromised patients face increased likelihood<br />

of developing nocardial infections. Defects in the mononuclear<br />

phagocyte system increase host susceptibility. The<br />

microorganisms grow in monocytes and macrophages. T<br />

cells of mice immunized against whole cells of Nocardia<br />

species become immunologically reactive against the<br />

microorganism and kill it directly. T cell-deficient athymic<br />

mice show increased susceptibility to nocardial infection,<br />

but B cell-deficient mice do not. Thus, T cells rather than B<br />

cells are critical for host immunity against nocardial infection.<br />

No effective vaccine against Nocardia is currently<br />

available.<br />

NOD (nonobese diabetic) mouse<br />

A mutant mouse strain that spontaneously develops type I<br />

insulin-dependent diabetes mellitus, an autoimmune disease;<br />

the strain exhibits an autosomal-recessive pattern of<br />

inheritance for the NOD mutation. Lymphocytes infiltrate<br />

NOD mouse islets of Langerhans in the pancreas and kill<br />

β cells. Humans with insulin-dependent diabetes mellitus<br />

have defects in the HLA-DQ parts of the major histocompatibility<br />

complex (MHC) class II region. There is also a<br />

defect in the class II IA region of murine MHC class II. A<br />

major DNA segment is missing from the NOD mouse MHC<br />

IE region. When the IE segment is inserted or the IA defect<br />

is corrected in these mice, disease progression is halted.<br />

This strain represents a significant animal model for human<br />

type I diabetes mellitus.<br />

NOD proteins<br />

Nucleotide-binding oligomerization domain proteins.<br />

Cytoplasmic pattern recognition molecules capable of<br />

detecting intracellular pathogen products. Related structurally<br />

to Toll-like receptors. NOD protein engagement leads<br />

to expression of pro-inflammatory cytokines.<br />

N

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