Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-10-5
pubmed:abstractText
BALB/c mice injected at birth with 10(8) (A/J X BALB/c)F1 hybrid spleen cells develop an autoimmune host-vs-graft (HVG) disease as a result of activation of donor B cells by host CD4+ cells. The antidonor CD4+ cells seem to be Th2-like cells, inasmuch as they are profoundly deficient in IL-2 and IFN-gamma production, but secrete high levels of IL-4 and IL-10. As IFN-gamma is known to inhibit the development of TH2 cells, we attempted to modulate HVG disease by injecting rIFN-gamma. First, we found that 10 micrograms of rIFN-gamma given on days 1 and 3 after birth reduced the serum hyper-IgE of HVG mice by 90% and the serum hyper-IgG1, by 70%. In addition, rIFN-gamma administration significantly decreased the anti-DNA IgG1 titers and prevented the occurrence of anti-glomerular basement membrane and anti-laminin IgG1 Abs as well as the formation of immune deposits in renal glomeruli. These effects were not caused by the abrogation of chimerism, as indicated by the persistence of donor-type B cells in lymph nodes and of Igs bearing donor allotype in serum. MLC experiments indicated that the major effect of early rIFN-gamma administration was to restore the production of IL-2 and IFN-gamma by donor-specific T cells while these cells still secreted significant amounts of IL-4 and IL-10. Unresponsiveness of antidonor cytolytic T cells was not influenced by rIFN-gamma. We conclude that rIFN-gamma prevents the TH2-type response induced by the neonatal injection of semiallogeneic spleen cells and the associated pathology.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
153
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2361-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8077653-Animals, pubmed-meshheading:8077653-Animals, Newborn, pubmed-meshheading:8077653-Antibodies, Antinuclear, pubmed-meshheading:8077653-Cytotoxicity Tests, Immunologic, pubmed-meshheading:8077653-Host vs Graft Reaction, pubmed-meshheading:8077653-Immunoglobulin Isotypes, pubmed-meshheading:8077653-Interferon-gamma, pubmed-meshheading:8077653-Kidney Diseases, pubmed-meshheading:8077653-Lymphocyte Culture Test, Mixed, pubmed-meshheading:8077653-Lymphocyte Transfusion, pubmed-meshheading:8077653-Lymphokines, pubmed-meshheading:8077653-Mice, pubmed-meshheading:8077653-Mice, Inbred BALB C, pubmed-meshheading:8077653-Mice, Inbred C57BL, pubmed-meshheading:8077653-Spleen, pubmed-meshheading:8077653-T-Lymphocytes, Helper-Inducer, pubmed-meshheading:8077653-Transplantation, Homologous, pubmed-meshheading:8077653-Transplantation Chimera
pubmed:year
1994
pubmed:articleTitle
IFN-gamma prevents Th2 cell-mediated pathology after neonatal injection of semiallogenic spleen cells in mice.
pubmed:affiliation
Interdisciplinary Laboratory of Experimental Biomedical Research Free University of Brussels, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't