Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 135, Issue 1-2, Pages 29-37Publisher
ELSEVIER
DOI: 10.1016/S0165-5728(02)00428-9
Keywords
apoptosis; autoimmune encephalomyelitis; cytokine; myelin oligodendrocyte glycoprotein; p53
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The role of p53, a pro-apoptotic protein, in experimental autoimmune encephalomyelitis (EAE) was investigated using p53-deficient C57BL/6J mice. p53-deficient mice immunised with myelin oligodendrocyte glycoprotein (MOG) exhibited a more severe clinical course of EAE with more severe inflammation in the central nervous system (CNS) compared to wild-type littermates. While T and B cell responses of p53-deficient mice to MOG were comparable to those of wild-type littermates, significantly higher production of IL-6, granulocyte macrophage colony-stimulating factor and IL-10 was observed in lymphocytes exposed to MOG from p53-deficient mice than those from wild-type littermates. Furthermore, a flow cytometric analysis of Annexin V staining showed that apoptosis of CNS-infiltrating cells was less in p53-deficient mice with EAE compared to wild-type littermates. These results suggest that p53 may be involved in the regulatory process of EAE through the control of cytokine production and/or the apoptotic elimination of inflammatory cells. (C) 2002 Elsevier Science B.V. All rights reserved.
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