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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1984-9-6
|
| pubmed:abstractText |
Seeking common abnormalities in mice genetically predisposed to lupus-like autoimmune disease, we investigated (1) the ontogeny of Ia antigens (I-A/I-E) on the surfaces of resident peritoneal macrophages (rpM phi) of lupus and normal mice, (2) spontaneous and lectin-induced in vitro production of M phi-stimulating factors (interferon, IFN; M phi-activating factor, MAF; M phi-Ia-inducing/recruiting factor, MIRF), and (3) responses of rpM phi from such animals to Ia-inducing signals. Indirect immunofluorescence techniques showed that Ia+ rpM phi increased numerically during the life spans of MRL/Mp lpr/lpr, while no such increase was observed in age-matched non-lpr MRL/Mp +/+ or (MRL/Mp lpr/lpr X MRL/Mp +/+)F1 hybrid mice. However, neonatal thymectomy, which prevents lymphoproliferation and autoimmune disease in MRL/Mp lpr/lpr mice, had no effect on this enhanced M phi I-A/I-E expression. NZB mice developed a similar increase with age, whereas BXSB and (NZB X NZW)F1 lupus mice, like immunologically normal controls, had low numbers of I-A/I-E+ rpM phi. Cultured splenocytes of lupus mice, including those with high percentages of I-A/I-E+ rpM phi, did not spontaneously (in the absence of mitogens) elaborate MIRF, MAF, or IFN activity. Furthermore, concanavalin A-stimulated splenocytes from lupus mice, particularly strains with early autoimmune disease manifestations [MRL/Mp lpr/lpr, male BXSB, and female (NZB X NZW)F1] produced levels of these lymphokines that were lower than normal controls. MRL/Mp lpr/lpr and NZB rpM phi, when stimulated in vitro with the supernatant of a MIRF-producing T cell hybridoma, did not hyperrespond. Our study shows that increased I-A/I-E+ rpM phi occur in some, but not all, lupus mice and this increase does not correlate with increased spontaneous or mitogen-induced production of M phi-stimulating lymphokines nor with hyperresponsiveness to Ia-inducing signals.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0008-8749
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
87
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
92-100
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:6204780-Aging,
pubmed-meshheading:6204780-Animals,
pubmed-meshheading:6204780-Female,
pubmed-meshheading:6204780-Genes, MHC Class II,
pubmed-meshheading:6204780-Histocompatibility Antigens Class II,
pubmed-meshheading:6204780-Interferons,
pubmed-meshheading:6204780-Lupus Erythematosus, Systemic,
pubmed-meshheading:6204780-Lymphocyte Activation,
pubmed-meshheading:6204780-Lymphokines,
pubmed-meshheading:6204780-Macrophage Activation,
pubmed-meshheading:6204780-Macrophage-Activating Factors,
pubmed-meshheading:6204780-Macrophages,
pubmed-meshheading:6204780-Male,
pubmed-meshheading:6204780-Mice,
pubmed-meshheading:6204780-Mice, Inbred BALB C,
pubmed-meshheading:6204780-Mice, Inbred C3H,
pubmed-meshheading:6204780-Mice, Inbred C57BL,
pubmed-meshheading:6204780-Mice, Inbred DBA,
pubmed-meshheading:6204780-Mice, Inbred NZB,
pubmed-meshheading:6204780-Mice, Mutant Strains
|
| pubmed:year |
1984
|
| pubmed:articleTitle |
Macrophage I-A/I-E expression and macrophage-stimulating lymphokines in murine lupus.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|