pVAXhsp65 Vaccination Primes for High IL-10 Production and Decreases Experimental Encephalomyelitis Severity.
Sofia Fernanda Gonçalves Zorzella-PezaventoFernanda Chiuso-MinicucciThais Graziela Donegá FrançaLarissa Lumi Watanabe IshikawaLarissa Camargo da RosaPriscila Maria ColaviteBianca BalbinoCamila MarquesMaura Rosane Valerio IkomaAna Paula MassonCélio Lopes SilvaAlexandrina SartoriPublished in: Journal of immunology research (2017)
Experimental autoimmune encephalomyelitis (EAE) is a demyelinating pathology of the central nervous system (CNS) used as a model to study multiple sclerosis immunopathology. EAE has also been extensively employed to evaluate potentially therapeutic schemes. Considering the presence of an immune response directed to heat shock proteins (hsps) in autoimmune diseases and the immunoregulatory potential of these molecules, we evaluated the effect of a previous immunization with a genetic vaccine containing the mycobacterial hsp65 gene on EAE development. C57BL/6 mice were immunized with 4 pVAXhsp65 doses and 14 days later were submitted to EAE induction by immunization with myelin oligodendrocyte glycoprotein (MOG35-55) emulsified in Complete Freund's Adjuvant. Vaccinated mice presented significant lower clinical scores and lost less body weight. MOG35-55 immunization also determined less inflammation in lumbar spinal cord but did not change CD4+CD25+Foxp3+ T cells frequency in spleen and CNS. Infiltrating cells from the CNS stimulated with rhsp65 produced significantly higher levels of IL-10. These results suggest that the ability of pVAXhsp65 vaccination to control EAE development is associated with IL-10 induction.
Keyphrases
- heat shock
- body weight
- multiple sclerosis
- spinal cord
- immune response
- heat shock protein
- heat stress
- blood brain barrier
- oxidative stress
- high fat diet induced
- regulatory t cells
- copy number
- multidrug resistant
- neuropathic pain
- white matter
- metabolic syndrome
- insulin resistance
- toll like receptor
- dendritic cells
- adipose tissue
- inflammatory response
- climate change
- cerebrospinal fluid
- risk assessment
- human health