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 journalArticle

15 Citations (Scopus)

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

Fingerprint

Autoimmune Experimental Encephalomyelitis
Immunization
Inflammation
Peptides
Central Nervous System
Acute Disease
Spontaneous Remission
T-Lymphocytes
Cyclooxygenase 2
Interleukin-4
Autoimmune Diseases
Multiple Sclerosis
Prostaglandins
Cytokines
Injections
myelin proteolipid protein (139-151)

Keywords

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

ASJC Scopus subject areas

  • Immunology

Cite this

Di Rosa, F., Serafini, B., Scognamiglio, P., Di Virgilio, A., Finocchi, L., Aloisi, F., & Barnaba, V. (2000). Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis. International Immunology, 12(5), 711-719.

Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis. / Di Rosa, Francesca; Serafini, Barbara; Scognamiglio, Paola; Di Virgilio, Antonio; Finocchi, Luigi; Aloisi, Francesca; Barnaba, Vincenzo.

In: International Immunology, Vol. 12, No. 5, 2000, p. 711-719.

Research output: Contribution to journalArticle

Di Rosa, F, Serafini, B, Scognamiglio, P, Di Virgilio, A, Finocchi, L, Aloisi, F & Barnaba, V 2000, 'Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis', International Immunology, vol. 12, no. 5, pp. 711-719.
Di Rosa, Francesca ; Serafini, Barbara ; Scognamiglio, Paola ; Di Virgilio, Antonio ; Finocchi, Luigi ; Aloisi, Francesca ; Barnaba, Vincenzo. / Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis. In: International Immunology. 2000 ; Vol. 12, No. 5. pp. 711-719.
@article{db6feeb22ee241a79471577d46af57b5,
title = "Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis",
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.",
keywords = "Adjuvant, Autoimmunity, Immunization, Inflammation, T cell cytokines",
author = "{Di Rosa}, Francesca and Barbara Serafini and Paola Scognamiglio and {Di Virgilio}, Antonio and Luigi Finocchi and Francesca Aloisi and Vincenzo Barnaba",
year = "2000",
language = "English",
volume = "12",
pages = "711--719",
journal = "International Immunology",
issn = "0953-8178",
publisher = "Oxford University Press",
number = "5",

}

TY - JOUR

T1 - Short-lived immunization site inflammation in self-limited active experimental allergic encephalomyelitis

AU - Di Rosa, Francesca

AU - Serafini, Barbara

AU - Scognamiglio, Paola

AU - Di Virgilio, Antonio

AU - Finocchi, Luigi

AU - Aloisi, Francesca

AU - Barnaba, Vincenzo

PY - 2000

Y1 - 2000

N2 - 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.

AB - 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.

KW - Adjuvant

KW - Autoimmunity

KW - Immunization

KW - Inflammation

KW - T cell cytokines

UR - http://www.scopus.com/inward/record.url?scp=0034018707&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034018707&partnerID=8YFLogxK

M3 - Article

C2 - 10784617

AN - SCOPUS:0034018707

VL - 12

SP - 711

EP - 719

JO - International Immunology

JF - International Immunology

SN - 0953-8178

IS - 5

ER -