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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1995-1-19
|
| pubmed:abstractText |
The scid mutation was backcrossed ten generations onto the NOD/Lt strain background, resulting in an immunodeficient stock (NOD/LtSz-scid/scid) with multiple defects in adaptive as well as nonadaptive immunologic function. NOD/LtSz-scid/scid mice lack functional lymphoid cells and show little or no serum Ig with age. Although NOD/(Lt-)+/+ mice develop T cell-mediated autoimmune, insulin-dependent diabetes mellitus, NOD/LtSz-scid/scid mice are both insulitis- and diabetes-free throughout life. However, because of a high incidence of thymic lymphomas, the mean lifespan of this congenic stock is only 8.5 mo under specific pathogen-free conditions. After i.v. injection of human CEM T-lymphoblastoid cells, splenic engraftment of these cells was fourfold greater in NOD/LtSz-scid/scid mice than in C.B17/Sz-scid/scid mice. Although C.B-17Sz-scid/scid mice exhibit robust NK cell activity, this activity is markedly reduced in both NOD/(Lt-)+/+ and NOD/LtSz-scid/scid mice. Presence of a functionally less mature macrophage population in NOD/LtSz-scid/scid vs C.B-17Sz-scid/scid mice is indicated by persistence in the former of the NOD/Lt strain-specific defect in LPS-stimulated IL-1 secretion by marrow-derived macrophages. Although C.B-17Sz-scid/scid and C57BL/6Sz-scid/scid mice have elevated serum hemolytic complement activity compared with their respective +/+ controls, both NOD/(LtSz-)+/+ and NOD/LtSz-scid/scid mice lack this activity. Age-dependent increases in serum Ig levels (> 1 micrograms/ml) were observed in only 2 of 30 NOD/LtSz-scid/scid mice vs 21 of 29 C.B-17/Sz-scid/scid animals. The multiple defects in innate and adaptive immunity unique to the NOD/LtSz-scid/scid mouse provide an excellent in vivo environment for reconstitution with human hematopoietic cells.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
154
|
| pubmed:geneSymbol |
Emv30
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
N
|
| pubmed:pagination |
180-91
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:7995938-Agammaglobulinemia,
pubmed-meshheading:7995938-Age Factors,
pubmed-meshheading:7995938-Animals,
pubmed-meshheading:7995938-Complement System Proteins,
pubmed-meshheading:7995938-Crosses, Genetic,
pubmed-meshheading:7995938-Diabetes Mellitus, Type 1,
pubmed-meshheading:7995938-Female,
pubmed-meshheading:7995938-Humans,
pubmed-meshheading:7995938-Immunity, Cellular,
pubmed-meshheading:7995938-Immunity, Innate,
pubmed-meshheading:7995938-Immunologic Deficiency Syndromes,
pubmed-meshheading:7995938-Immunophenotyping,
pubmed-meshheading:7995938-Interleukin-1,
pubmed-meshheading:7995938-Killer Cells, Natural,
pubmed-meshheading:7995938-Leukocyte Count,
pubmed-meshheading:7995938-Lipopolysaccharides,
pubmed-meshheading:7995938-Longevity,
pubmed-meshheading:7995938-Lymphoid Tissue,
pubmed-meshheading:7995938-Lymphoma,
pubmed-meshheading:7995938-Macrophage Activation,
pubmed-meshheading:7995938-Macrophages,
pubmed-meshheading:7995938-Male,
pubmed-meshheading:7995938-Mice,
pubmed-meshheading:7995938-Mice, Inbred NOD,
pubmed-meshheading:7995938-Mice, Mutant Strains,
pubmed-meshheading:7995938-Mice, SCID,
pubmed-meshheading:7995938-Poly I-C,
pubmed-meshheading:7995938-Severe Combined Immunodeficiency,
pubmed-meshheading:7995938-Skin Transplantation,
pubmed-meshheading:7995938-T-Lymphocytes,
pubmed-meshheading:7995938-Thymus Neoplasms,
pubmed-meshheading:7995938-Transplantation, Heterologous
|
| pubmed:year |
1995
|
| pubmed:articleTitle |
Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice.
|
| pubmed:affiliation |
Jackson Laboratory, Bar Harbor, ME 04609.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|