Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
1989-10-20
|
| pubmed:abstractText |
The induction of transplantation tolerance to H-2b alloantigens in BALB/c (H-2d) mice by neonatal injection of (C57BL/6 x BALB/c)F1 spleen cells, produces an autoimmune lupus-like syndrome due to an activation of persisting F1 donor B cells. This syndrome is characterized by hypergammaglobulinaemia, high levels of anti-DNA antibodies, as well as by circulating immune complexes and glomerular deposits of Ig. The role of host T cells in this model was investigated by using athymic BALB/c nu/nu mice as recipients of normal (C57BL/6 x BALB.Igb)F1 spleen cells. In these "tolerized" BALB/c nu/nu mice, there was a persistence of F1 donor B cells but none of the autoimmune features were expressed, conversely to tolerized BALB/c nu/+ littermates. The injection of CD4+CD8- T lymphocytes from adult normal BALB/c mice in 3-wk-old tolerized BALB/c nu/nu mice triggered the appearance of all the autoimmune findings observed in euthymic tolerant mice. The autoantibodies were produced by persisting F1 donor B cells as shown by allotype analysis. More strikingly, a similar triggering of the autoimmune syndrome, including high titers of anti-DNA IgG antibodies and circulating immune complexes, was observed after injection of CD4+CD8- T cells from 2-wk-old tolerant BALB/c mice into "tolerized" BALB/c nu/nu mice. The anti-ssDNA antibodies were shown to bear only the Ighb allotype, indicating their exclusive origin from F1 donor B cells. These results imply that CD4+ T cells from the tolerant mice are necessary for the activation of autoreactive F1 B cells and for the development of the autoimmune syndrome occurring in this model. They also suggest that, although there is a marked depletion of H-2b-specific alloreactive CTL precursors in those neonatally tolerized mice, this state of tolerance can be associated with the persistence of H-2b-specific alloreactive CD4+ cells.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Antinuclear,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Single-Stranded,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Allotypes,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Isotypes,
http://linkedlifedata.com/resource/pubmed/chemical/Isoantigens
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
143
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
2202-8
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:2570803-Animals,
pubmed-meshheading:2570803-Animals, Newborn,
pubmed-meshheading:2570803-Antibodies, Antinuclear,
pubmed-meshheading:2570803-Autoimmune Diseases,
pubmed-meshheading:2570803-B-Lymphocytes,
pubmed-meshheading:2570803-CD4-Positive T-Lymphocytes,
pubmed-meshheading:2570803-Crosses, Genetic,
pubmed-meshheading:2570803-DNA, Single-Stranded,
pubmed-meshheading:2570803-Female,
pubmed-meshheading:2570803-Immune Tolerance,
pubmed-meshheading:2570803-Immunoglobulin Allotypes,
pubmed-meshheading:2570803-Immunoglobulin Isotypes,
pubmed-meshheading:2570803-Isoantigens,
pubmed-meshheading:2570803-Lymphocyte Activation,
pubmed-meshheading:2570803-Male,
pubmed-meshheading:2570803-Mice,
pubmed-meshheading:2570803-Mice, Inbred BALB C,
pubmed-meshheading:2570803-Mice, Inbred C57BL,
pubmed-meshheading:2570803-Mice, Nude,
pubmed-meshheading:2570803-Syndrome
|
| pubmed:year |
1989
|
| pubmed:articleTitle |
Autoimmune syndrome after induction of neonatal tolerance to alloantigens. CD4+ T cells from the tolerant host activate autoreactive F1 B cells.
|
| pubmed:affiliation |
WHO Immunology Research and Training Centre, Department of Pathology, Geneva, Switzerland.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|