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-gamma-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.
authors.affiliation: Fondazione Andrea Cesalpino, Istituto I Clinica Medica, Università 'La Sapienza', Rome 00161, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Di Rosa
authors.forename: B
authors.initials: B
authors.lastname: Serafini
authors.forename: P
authors.initials: P
authors.lastname: Scognamiglio
authors.forename: A
authors.initials: A
authors.lastname: Di Virgilio
authors.forename: L
authors.initials: L
authors.lastname: Finocchi
authors.forename: F
authors.initials: F
authors.lastname: Aloisi
authors.forename: V
authors.initials: V
authors.lastname: Barnaba
mesh_terms: D000208:Acute Disease; D000818:Animals; D015703:Antigens, CD; D018845:CD11 Antigens / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis; D002490:Central Nervous System / Q000276:immunology; D051546:Cyclooxygenase 2; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000276:immunology*; D005260:Female; D007114:Immunization; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins / Q000032:analysis; D051379:Mice; D015778:Minor Histocompatibility Antigens; D018991:Myelin Proteolipid Protein; D010446:Peptide Fragments; D011451:Prostaglandin-Endoperoxide Synthases / Q000032:analysis; D011956:Receptors, Cell Surface / Q000032:analysis; D012867:Skin / Q000276:immunology; D013116:Spinal Cord / Q000276:immunology; D013997:Time Factors
chemical_list: D015703:Antigens, CD; D018845:CD11 Antigens; D015704:CD4 Antigens; C093569:DEC-205 receptor; D007527:Isoenzymes; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D015778:Minor Histocompatibility Antigens; D018991:Myelin Proteolipid Protein; D010446:Peptide Fragments; D011956:Receptors, Cell Surface; C435023:myelin proteolipid protein (139-151); D015847:Interleukin-4; D007371:Interferon-gamma; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases