Passive collagen arthritis induced by anticollagen igg

Suresh S. Kerwar, Arnold L. Oronsky

Research output: Contribution to journalArticle

Abstract

Studies conducted in rats and mice indicate that passive arthritis can be transferred to naive recipients with anticollagen IgG. The passively transferred disease is less severe and is transient. Rats that recover from passive arthritis are resistant to a second phase of clinical disease when administered either anticollagen IgG or type II collagen. Suppressor T cells appear to be responsible for this resistance. Passive arthritis induced by anticollagen IgG is a complement dependent lesion. Deposition of IgG on the cartilage and host complement C3 and C5 activation are essential for the induction of passive disease. Inflammatory cells are necessary for the demonstration of passive arthritis; mice deficient in inflammatory cells or defective in this cell population are resistant to passive arthritis. Monoclonal antibodies reactive to type II collagen or to a renatured TCA fragment can also induce passive arthritis. The disease is subclinical and can be detected only after histological analysis of the joints.

Original languageEnglish (US)
Pages (from-to)17-23
Number of pages7
JournalInternational Reviews of Immunology
Volume4
Issue number1
DOIs
StatePublished - 1988
Externally publishedYes

Fingerprint

Experimental Arthritis
Arthritis
Immunoglobulin G
Collagen Type II
Complement C5
Complement C3
Cartilage
Joints
Monoclonal Antibodies
T-Lymphocytes
Population

Keywords

  • Anticollagen IgG
  • Complement
  • Monoclonal antitype II collagen antibodies
  • Passive arthritis
  • T suppressor cells

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Passive collagen arthritis induced by anticollagen igg. / Kerwar, Suresh S.; Oronsky, Arnold L.

In: International Reviews of Immunology, Vol. 4, No. 1, 1988, p. 17-23.

Research output: Contribution to journalArticle

Kerwar, Suresh S. ; Oronsky, Arnold L. / Passive collagen arthritis induced by anticollagen igg. In: International Reviews of Immunology. 1988 ; Vol. 4, No. 1. pp. 17-23.
@article{e1b9099c86dc4ccda5e5cd58bc6b0f11,
title = "Passive collagen arthritis induced by anticollagen igg",
abstract = "Studies conducted in rats and mice indicate that passive arthritis can be transferred to naive recipients with anticollagen IgG. The passively transferred disease is less severe and is transient. Rats that recover from passive arthritis are resistant to a second phase of clinical disease when administered either anticollagen IgG or type II collagen. Suppressor T cells appear to be responsible for this resistance. Passive arthritis induced by anticollagen IgG is a complement dependent lesion. Deposition of IgG on the cartilage and host complement C3 and C5 activation are essential for the induction of passive disease. Inflammatory cells are necessary for the demonstration of passive arthritis; mice deficient in inflammatory cells or defective in this cell population are resistant to passive arthritis. Monoclonal antibodies reactive to type II collagen or to a renatured TCA fragment can also induce passive arthritis. The disease is subclinical and can be detected only after histological analysis of the joints.",
keywords = "Anticollagen IgG, Complement, Monoclonal antitype II collagen antibodies, Passive arthritis, T suppressor cells",
author = "Kerwar, {Suresh S.} and Oronsky, {Arnold L.}",
year = "1988",
doi = "10.3109/08830188809044767",
language = "English (US)",
volume = "4",
pages = "17--23",
journal = "International Reviews of Immunology",
issn = "0883-0185",
publisher = "Informa Healthcare",
number = "1",

}

TY - JOUR

T1 - Passive collagen arthritis induced by anticollagen igg

AU - Kerwar, Suresh S.

AU - Oronsky, Arnold L.

PY - 1988

Y1 - 1988

N2 - Studies conducted in rats and mice indicate that passive arthritis can be transferred to naive recipients with anticollagen IgG. The passively transferred disease is less severe and is transient. Rats that recover from passive arthritis are resistant to a second phase of clinical disease when administered either anticollagen IgG or type II collagen. Suppressor T cells appear to be responsible for this resistance. Passive arthritis induced by anticollagen IgG is a complement dependent lesion. Deposition of IgG on the cartilage and host complement C3 and C5 activation are essential for the induction of passive disease. Inflammatory cells are necessary for the demonstration of passive arthritis; mice deficient in inflammatory cells or defective in this cell population are resistant to passive arthritis. Monoclonal antibodies reactive to type II collagen or to a renatured TCA fragment can also induce passive arthritis. The disease is subclinical and can be detected only after histological analysis of the joints.

AB - Studies conducted in rats and mice indicate that passive arthritis can be transferred to naive recipients with anticollagen IgG. The passively transferred disease is less severe and is transient. Rats that recover from passive arthritis are resistant to a second phase of clinical disease when administered either anticollagen IgG or type II collagen. Suppressor T cells appear to be responsible for this resistance. Passive arthritis induced by anticollagen IgG is a complement dependent lesion. Deposition of IgG on the cartilage and host complement C3 and C5 activation are essential for the induction of passive disease. Inflammatory cells are necessary for the demonstration of passive arthritis; mice deficient in inflammatory cells or defective in this cell population are resistant to passive arthritis. Monoclonal antibodies reactive to type II collagen or to a renatured TCA fragment can also induce passive arthritis. The disease is subclinical and can be detected only after histological analysis of the joints.

KW - Anticollagen IgG

KW - Complement

KW - Monoclonal antitype II collagen antibodies

KW - Passive arthritis

KW - T suppressor cells

UR - http://www.scopus.com/inward/record.url?scp=0024084641&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024084641&partnerID=8YFLogxK

U2 - 10.3109/08830188809044767

DO - 10.3109/08830188809044767

M3 - Article

C2 - 3072383

AN - SCOPUS:0024084641

VL - 4

SP - 17

EP - 23

JO - International Reviews of Immunology

JF - International Reviews of Immunology

SN - 0883-0185

IS - 1

ER -