Augmented expression of Daintain/allograft inflammatory factor-1 is associated with clinical disease: Dynamics of Daintain/allograft inflammatory factor-1 expression in spleen, peripheral nerves and sera during experimental autoimmune neuritis

Citation
M. Pashenkov et al., Augmented expression of Daintain/allograft inflammatory factor-1 is associated with clinical disease: Dynamics of Daintain/allograft inflammatory factor-1 expression in spleen, peripheral nerves and sera during experimental autoimmune neuritis, SC J IMMUN, 52(2), 2000, pp. 117-122
Citations number
21
Categorie Soggetti
Immunology
Journal title
SCANDINAVIAN JOURNAL OF IMMUNOLOGY
ISSN journal
03009475 → ACNP
Volume
52
Issue
2
Year of publication
2000
Pages
117 - 122
Database
ISI
SICI code
0300-9475(200008)52:2<117:AEODIF>2.0.ZU;2-O
Abstract
Experimental autoimmune neuritis (EAN) is an animal model of Guillain-Barre syndrome, characterized by inflammation and demyelination of the periphera l nervous system (PNS). Daintain/allograft inflammatory factor-1 (daintain/ AIF-1) is a novel interferon-gamma-inducible protein expressed by macrophag es during organ specific autoimmune diseases. To study the involvement of d aintain/AIF-1 in EAN we induced EAN in Lewis rats by immunizing with bovine PNS myelin (BPM) and complete Freund's adjuvant (CFA). The expression of d aintain/AIF-1 was examined in the spleen, peripheral nerves and sera during the course of EAN by immunohistochemistry and radioimunoassay (RIA). The e xpression of daintain/AIF-1 in the spleen and in the sciatic nerves peaked at the preclinical stage (day 7 post immunization (p.i.)) and at the height (day 15 p.i.) of clinical EAN, consistent with a disease promoting role fo r daintain/AIF-1. Daintain/AIF-1 expressing cells represented a subset of E D1(+) or CD11b/c(+) mononuclear cells. A significant increase of daintain/A IF-1-like immunoreactivity in sera occurred at the preclinical stage of EAN . Taken together, these data indicate that daintain/AIF-1 may play a proinf lammatory role in the pathogenesis of EAN.