Breast regression protein-39 is not required for experimental autoimmune encephalomyelitis induction

Ester Cantó, Carmen Espejo, Carme Costa, Xavier Montalban, Manuel Comabella

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2 Citations (Scopus)


© 2015 Elsevier Inc. Increasing evidence points to a role for chitinase 3-like 1 (CHI3L1) in multiple sclerosis (MS). Here, we aimed to explore the potential involvement of CHI3L1 in the animal model of MS, experimental autoimmune encephalomyelitis (EAE). EAE was induced by immunization with MOG35-55 peptide in wild-type (WT) and knock-out (KO) mice for breast regression protein 39 (BRP-39), the mouse homologue of human CHI3L1. Immunological responses in splenocytes were assessed by means of polyclonal and antigen-specific proliferation assays. Central nervous system pathology and chitinase gene expression were also investigated. BRP-39 expression was increased in WT MOG35-55-immunized mice compared to saline-immunized controls. No differences were found between WT and BRP-39 KO mice regarding EAE clinical course, day of disease onset, mortality rate, splenocyte proliferative responses or histopathological findings. These results do not support a role of BRP-39 in the pathogenesis of EAE.
Original languageEnglish
Pages (from-to)133-141
JournalClinical Immunology
Issue number2
Publication statusPublished - 1 Oct 2015


  • BRP-39
  • EAE
  • Multiple sclerosis


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