Journal of neuroimmunology
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To determine the role of gene-environmental interactions between the Class I and Class II HLA alleles and the humoral anti-Epstein-Barr Virus (EBV) responses in the development of brain injury and clinical disability in multiple sclerosis (MS) patients. ⋯ Our data suggest that gene-environment interactions between specific HLA Class I loci and EBV exposure are associated with MRI markers of lesion injury and brain atrophy in MS patients.
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We have revealed that local stimulation of sensory neurons is involved in the adjuvant effect of dibutyl phthalate (DBP) in a fluorescein isothiocyanate-induced mouse contact hypersensitivity model. Transient receptor potential (TRP) A1 and TRPV1 seemed to be candidate DBP targets. ⋯ TRPA1 and TRPV1 activation was further demonstrated using cultured cells expressing TRP channels. Among structurally different phthalate esters, there is a positive relationship between the activation of TRPA1- or TRPV1-expressing cells and the adjuvant effect.
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Myasthenia gravis (MG), a prototypic antibody-mediated autoimmune disease, presents an excellent target for scientific research aimed at a better understanding of the disease itself and the source that triggers an autoimmune reaction in an organism. MG is a neuromuscular disease caused mainly by an autoimmune response against the nicotinic acetylcholine receptor (AChR) which interferes with neuromuscular transmission. ⋯ This review is dedicated to the late Prof. John Newsom-Davis, who was the first to introduce the use of plasmapheresis for MG.
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We compared the effects of peripheral Freund's Complete Adjuvant (CFA) and formalin injection on spinal microglia activation. Both qualitative and quantitative analyses showed signs of microglia activation on the ipsilateral side of the lumbar dorsal horn on day 3, day 7 and day 14 after formalin injection. ⋯ At the injection site in the paw, CFA injection induced considerably more inflammation than formalin injection. Although spinal microglia might be activated in inflammatory pain models, morphologically, spinal microglia activation was not closely correlated with peripheral inflammation.
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Gene regulation in sepsis is known to be controlled by the transcription factor NF-kappaB. However, the function of neuronal NF-kappaB in sepsis is not well defined. In a mouse model of sepsis induced by i.p. injection of lipopolysaccharides (LPS), we found an activation of NF-kappaB in the brain as shown by the induction of a transgenic NF-kappaB reporter. ⋯ By immunohistochemistry, we detected the active NF-kappaB subunit RelA in neuronal nuclei of the organum vasculosum of the lamina terminalis. Our data reveal an important role of neuronal NF-kappaB in thermoregulation and survival. The upcoming group of NF-kappaB inhibitors may have a place in the treatment of the acute-phase response.