| Autor: |
Chung JY; Department of Immunology, Central Clinical School, Monash University, Melbourne, Victoria 3181, Australia;, Figgett W, Fairfax K, Bernard C, Chan J, Toh BH, Mackay F, Alderuccio F |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2014 Mar 15; Vol. 192 (6), pp. 2593-601. Date of Electronic Publication: 2014 Feb 14. |
| DOI: |
10.4049/jimmunol.1203563 |
| Abstrakt: |
The various mechanisms that have been described for immune tolerance govern our ability to control self-reactivity and minimize autoimmunity. However, the capacity to genetically manipulate the immune system provides a powerful avenue to supplement this natural tolerance in an Ag-specific manner. We have previously shown in the mouse model of experimental autoimmune encephalomyelitis that transfer of bone marrow (BM) transduced with retrovirus encoding myelin oligodendrocyte glycoprotein (MOG) promotes disease resistance and CD4(+) T cell deletion within the thymus. However, the consequence of this strategy on B cell tolerance is not known. Using BM from IgH(MOG) mice that develop MOG-specific B cell receptors, we generated mixed chimeras together with BM-encoding MOG. In these animals, the development of MOG-specific B cells was abrogated, resulting in a lack of MOG-specific B cells in all B cell compartments examined. This finding adds a further dimension to our understanding of the mechanisms of tolerance that are associated with this gene therapy approach to treating autoimmunity and may have important implications for Ab-mediated autoimmune disorders. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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