Abstract
Minocycline Down-regulates MHC II Expression in Microglia and Macrophages through Inhibition of IRF-1 and Protein Kinase C (PKC)α/βII
Highlights
15208 JOURNAL OF BIOLOGICAL CHEMISTRY characterized by T cell-mediated inflammation, demyelination, and axonal loss in the central nervous system (CNS)
We have previously shown that minocycline ameliorated the clinical course of EAE and decreased major histocompatibility complex class II (MHC II) expression in the spinal cord [13]; the exact molecular mechanisms underlying these anti-inflammatory effects of minocycline remain unknown
Minocycline Decreases MHC II Expression in EAE—MOGinduced EAE in Dark Agouti rats is characterized by severe inflammatory lesions found predominantly in the spinal cord accompanied by a strong microglial response
Summary
15208 JOURNAL OF BIOLOGICAL CHEMISTRY characterized by T cell-mediated inflammation, demyelination, and axonal loss in the CNS. After priming of encephalitogenic T cells in the periphery, they migrate into the CNS, where they trigger inflammatory responses including microglial activation. To sustain their activation, the self-reactive T cells have to be reactivated in the CNS by encountering their cognate antigen bound to MHC II. The resident innate immune cells of the CNS, have been shown to be the main antigen-presenting cells of the CNS [3, 4] They normally express low levels of MHC II proteins; in inflammatory or neurodegenerative conditions, activated microglia highly up-regulate MHC II and co-stimulatory molecules [5]. Our data reveal that minocycline inhibits MHC II expression in microglia via the inhibition of CIITA expression by a mechanism involving the inhibition of IFN␥ regulatory factor (IRF-1) translocation to the nucleus in a PKC␣/-dependent manner
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