Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis

Francesca Di Rosa, Barbara Serafini, Paola Scognamiglio, Antonio Di Virgilio, Luigi Finocchi, Francesca Aloisi, Vincenzo Barnaba

Research output: Contribution to journalArticlepeer-review

Abstract

To understand the mechanisms underlying spontaneous remission of proteolipid protein (PLP) 139-151 peptide-induced experimental allergic encephalomyelitis (EAE), an acute autoimmune disease of SJL mice resembling human multiple sclerosis, we examined both the effector response site in the central nervous system (CNS) and the immunization site at different phases of the disease. In the CNS, the frequency of PLP 139-151 peptide-specific IFN-γ-producing T cells as well as the amount of infiltrating CD4+ and CD11b+ cells decreased with recovery. However, IL-4-producing cells were always rare and cyclooxygenase-2+ cells were numerous only at disease peak in the CNS, suggesting that T(h)2 cytokines and prostaglandins did not determine remission of EAE. By looking at the s.c. site of PLP 139-151 peptide plus adjuvant injection, we found that, although the inflammatory infiltrate was abundant, CD11b+ cells started to decrease already during disease acute phase and DEC-205+ cells were numerous only at early time points. We propose that immunization site inflammation is short-lived in PLP 139-151 peptide-induced EAE, and this leads to a temporary autoreactive T cell stimulation and to a self-limited disease.

Original languageEnglish
Pages (from-to)711-719
Number of pages9
JournalInternational Immunology
Volume12
Issue number5
Publication statusPublished - 2000

Keywords

  • Adjuvant
  • Autoimmunity
  • Immunization
  • Inflammation
  • T cell cytokines

ASJC Scopus subject areas

  • Immunology

Fingerprint Dive into the research topics of 'Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis'. Together they form a unique fingerprint.

Cite this