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Uncoupling protein 2 has protective function during experimental autoimmune encephalomyelitis.

Abstract : Uncoupling protein 2 (UCP2) is a member of the mitochondrial transporter superfamily that is expressed in many tissues, including immune cells. UCP2 prevents oxidative stress by reducing reactive oxygen species. Using UCP2-deficient mice, it was shown that UCP2 is involved in the regulation of insulin secretion, in the resistance to infection, and in atherosclerosis. Here, we investigated the role of UCP2 in experimental autoimmune encephalomyelitis, a murine model of multiple sclerosis. Immunized C57BL/6J UCP2-deficient mice showed a slightly delayed onset during experimental autoimmune encephalomyelitis (13.0 +/- 0.6 versus 11.5 +/- 0.8 in wild-type controls) and developed significantly higher disease scores than littermate controls (maximum disease score of 2.9 +/- 0.2 versus 1.7 +/- 0.2, P = 0.001). Higher levels of infiltrating T cells into the spinal cord meninges and parenchyma were observed. The T-cell proliferative response to the specific antigen was increased in UCP2-deficient mice compared with littermate controls, and CD4 cells of UCP2 knockout mice produced significantly higher levels of pro-inflammatory cytokines, eg, tumor necrosis factor-alpha and interleukin-2, resulting from a Th1 response. Mice lacking UCP2 also developed a higher B-cell response. Concomitantly, CD4 and CD8 cells of the UCP2-deficient mice showed increased production of reactive oxygen species. These results suggest a protective function of UCP2 in chronic inflammatory diseases such as multiple sclerosis.
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Contributor : Patricia Meralli Connect in order to contact the contributor
Submitted on : Monday, March 12, 2007 - 4:58:03 PM
Last modification on : Friday, January 8, 2021 - 4:54:06 PM


  • HAL Id : hal-00136181, version 1
  • PUBMED : 16651623



Susanne Vogler, Jens Pahnke, Sophie Rousset, Daniel Ricquier, Holger Moch, et al.. Uncoupling protein 2 has protective function during experimental autoimmune encephalomyelitis.. American Journal of Pathology, American Society for Investigative Pathology, 2006, 168 (5), pp.1570-5. ⟨hal-00136181⟩



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