Abstract
Xenotransplantation of rat bone marrow cells (BMC) into immunodeficient (SCID) mice generates chimeric mice susceptible to paralytic autoimmune CNS inflammation. Herein, we identified a disease relevant subset of transplantable BMC lacking expression of CD11b/c and CD49d. Moreover, disease susceptibility was enhanced in the presence of non-myelin specific T-cells. Only the CD11b/c negative population of BM retained the capability to populate the blood, spleen and spinal cord of recipients and matured after transplant to express CD11b/c. These results indicate non-myelin T cells in combination with integrin negative BM represent pre-pathogenic determinants of an enhanced disease susceptibility to myelin reactive T cells.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Bone Marrow Cells
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Bone Marrow Transplantation / methods*
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CD11b Antigen / immunology
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CD11b Antigen / metabolism
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CD11c Antigen / immunology
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CD11c Antigen / metabolism
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Cell Transplantation / methods
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Chimera
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Disease Models, Animal
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Disease Susceptibility
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Encephalomyelitis, Autoimmune, Experimental / immunology
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Encephalomyelitis, Autoimmune, Experimental / surgery*
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Female
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Immunophenotyping / methods
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Integrin alpha1 / metabolism
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Integrins / deficiency*
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Mice
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Mice, SCID
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Rats
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Rats, Inbred Lew
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Severity of Illness Index
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Transplantation, Heterologous / methods*
Substances
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CD11b Antigen
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CD11c Antigen
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Integrin alpha1
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Integrins