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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1990-4-30
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pubmed:abstractText |
Analysis of the capacity of splenocytes from non-prototypic Mlsa or Mlsc mouse strains to stimulate allogeneic H-2k-compatible T cells in a primary Mls-defined MLR provided interesting examples of exceptions to the usually stated characterization of Mlsa and Mlsc determinants as highly stimulatory of weakly stimulatory, respectively. Across the Mlsa barrier, MA/My stimulator cells had a significantly reduced capacity to elicit responder proliferation in comparison with prototypic AKR/J or less well studied C58/J, CE/J, or RF/J splenocytes. Across the Mlsc barrier, a gradient of stimulatory ability was observed with RF/J splenocytes being virtually nonstimulatory, prototypic C3H/HeJ splenocytes having an intermediate capacity, and CE/J and C58/J being highly stimulatory presenters of this non-MHC specificity. The differing capacity of each of these H-2k stimulator cells to elicit unprimed responder cell proliferation across an Mlsa or Mlsc difference correlated with the T cell growth factor activity that was secreted into the MLR supernatants. The super stimulatory form of Mlsc was expressed in an autosomal dominant fashion by (Mlsc poorly stimulatory x Mlsc super-stimulatory)F1 animals, (BALB.K x C58/J)F1 or (RF/J x CE/J)F1. The segregation of Mlsc stimulatory ability among first backcross and F2 animals derived from the former F1 was compatible with a single non-MHC gene controlling the expression and presentation of the super-stimulatory form of Mlsc. The regulatory nature of this gene was indicated by the observation that F1 animals generated from the Mlsc nonprototypic and poorly stimulatory BALB/c parental strain were self-tolerant to the super-stimulatory form of Mlsc. The existence of an Mls specificity other than a and c was suggested by positive non-MHC MLR responses in certain responder/stimulator cell combinations of Mls prototypic and nonprototypic mouse strains.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
144
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2506-17
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2138649-Animals,
pubmed-meshheading:2138649-Antigen-Presenting Cells,
pubmed-meshheading:2138649-Antigens, Surface,
pubmed-meshheading:2138649-B-Lymphocytes,
pubmed-meshheading:2138649-Genes, MHC Class II,
pubmed-meshheading:2138649-Immune Tolerance,
pubmed-meshheading:2138649-Immunologic Deficiency Syndromes,
pubmed-meshheading:2138649-Interleukin-2,
pubmed-meshheading:2138649-Interleukin-4,
pubmed-meshheading:2138649-Lymphocyte Activation,
pubmed-meshheading:2138649-Lymphocyte Culture Test, Mixed,
pubmed-meshheading:2138649-Lymphocytes,
pubmed-meshheading:2138649-Mice,
pubmed-meshheading:2138649-Mice, Inbred Strains,
pubmed-meshheading:2138649-Minor Lymphocyte Stimulatory Antigens,
pubmed-meshheading:2138649-Spleen
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pubmed:year |
1990
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pubmed:articleTitle |
Genetic analysis of the presentation of minor lymphocyte-stimulating determinants. II. Differing non-MHC control of super-stimulatory and more poorly stimulatory Mls phenotypes.
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pubmed:affiliation |
Immunobiology and Transplantation Department, Naval Medical Research Institute, Bethesda, MD 20814-5055.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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