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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0035015,
umls-concept:C0039194,
umls-concept:C0085112,
umls-concept:C0085358,
umls-concept:C0450127,
umls-concept:C0680727,
umls-concept:C1123023,
umls-concept:C1332714,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1548437,
umls-concept:C1706438,
umls-concept:C1882923,
umls-concept:C2698600
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pubmed:issue |
2
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pubmed:dateCreated |
1992-9-8
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pubmed:abstractText |
We analyzed the role of CD4+ and CD8+ T cells in H-2-disparate skin allograft rejection in the mutant mouse strain C.B-17/Icr scid with severe combined immunodeficiency. On the day of skin allografting, scid mice were adoptively transferred with negatively selected CD4+ or CD8+ splenocytes from normal unsensitized C.B-17/Icr mice. These populations were obtained using a double-mAb--plus--complement elimination protocol using anti-CD4 or anti-CD8 mAb that resulted in no detectable CD4+ or CD8+ cells by FACS and negligible numbers of cytolytic T lymphocytes by limiting dilution analysis in anti-CD8 treated populations. Spleen cells were removed from grafted mice at the time of rejection and were tested in vitro for antidonor reactivity in several assays: mixed lymphocyte culture, cell-mediated lympholysis, and LDA for CTL and for IL-2-producing HTL. The presence of Thy 1.2+, CD4+, or CD8+ cells was determined by FACS. All control C.B-17 mice and scid mice adoptively transferred with nondepleted CD4+, and CD8+ cells rejected skin allografts with similar mean survival times (15.6 +/- 1.5, 18.8 +/- 3.4, 18.0 +/- 5.4, respectively), whereas control scid mice retain skin allografts indefinitely (all greater than 100 days). C.B-17 syngeneic grafts survived indefinitely in all groups. At the time of rejection, splenocytes from scid mice receiving CD4+ cells had negligible donor-specific cytotoxicity in CML and negligible numbers of CTL by LDA, but demonstrated a good proliferative response in MLC and IL-2-producing cells by LDA (frequency = 1/1764). There were no detectable CD8+ cells present by FACS analysis. Conversely, splenocytes from scid mice adoptively transferred with CD8+ cells had strong donor-specific cytotoxicity in CML (58.8% +/- 16.1%) and CTL by LDA (frequency = 1/3448), but no significant proliferation was detected in MLC. There were no detectable CD4+ cells by FACS, but there were small numbers of IL-2-producing cells by LDA (frequency = 1/10,204). These data demonstrate that CD4+ cells adoptively transferred into scid mice are capable of mediating skin allograft rejection in the absence of any detectable CD8+ cells or significant functional cytolytic activity. The adoptive transfer of CD8+ cells also results in skin allograft rejection in the absence of detectable CD4+ cells. The detection of small numbers of IL-2 secreting cells in these mice may indicate that CD(8+)-mediated allograft rejection in this model is dependent on IL-2-secreting CD8+ cells.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0041-1337
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
278-86
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1353912-Animals,
pubmed-meshheading:1353912-Antigens, CD8,
pubmed-meshheading:1353912-CD4-Positive T-Lymphocytes,
pubmed-meshheading:1353912-Flow Cytometry,
pubmed-meshheading:1353912-Graft Rejection,
pubmed-meshheading:1353912-H-2 Antigens,
pubmed-meshheading:1353912-Immunization, Passive,
pubmed-meshheading:1353912-Interleukin-2,
pubmed-meshheading:1353912-Lymphocyte Culture Test, Mixed,
pubmed-meshheading:1353912-Mice,
pubmed-meshheading:1353912-Mice, SCID,
pubmed-meshheading:1353912-Skin Transplantation,
pubmed-meshheading:1353912-T-Lymphocyte Subsets,
pubmed-meshheading:1353912-T-Lymphocytes, Cytotoxic
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pubmed:year |
1992
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pubmed:articleTitle |
Mediation of skin allograft rejection in scid mice by CD4+ and CD8+ T cells.
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pubmed:affiliation |
Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63110.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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