Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology

T. F. Kresina, Jung Yoo, V. M. Goldberg

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

We examined antiproteoglycan antibodies as an autoimmune response for induction of synovitis. This hypothesis was studied by monitoring humoral antiproteoglycan antibody following IgG induction of experimental immuno synovitis, localization in the articular cartilage of an autologous immune response, and loss of proteoglycan from cartilage following intravenous administration of antiproteoglycan monoclonal antibodies. The data support the hypothesis that autoimmunity to cartilage macromolecules may play a role in the etiopathogenesis of arthritis.

Original languageEnglish (US)
Pages (from-to)248-257
Number of pages10
JournalArthritis and Rheumatism
Volume31
Issue number2
StatePublished - 1988

Fingerprint

Synovitis
Proteoglycans
Humoral Immunity
Autoimmunity
Cartilage
Pathology
Antibodies
Articular Cartilage
Intravenous Administration
Arthritis
Immunoglobulin G
Monoclonal Antibodies

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

Cite this

Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology. / Kresina, T. F.; Yoo, Jung; Goldberg, V. M.

In: Arthritis and Rheumatism, Vol. 31, No. 2, 1988, p. 248-257.

Research output: Contribution to journalArticle

@article{1dacf2eb4f394c11b2a62564bbf6c96d,
title = "Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology",
abstract = "We examined antiproteoglycan antibodies as an autoimmune response for induction of synovitis. This hypothesis was studied by monitoring humoral antiproteoglycan antibody following IgG induction of experimental immuno synovitis, localization in the articular cartilage of an autologous immune response, and loss of proteoglycan from cartilage following intravenous administration of antiproteoglycan monoclonal antibodies. The data support the hypothesis that autoimmunity to cartilage macromolecules may play a role in the etiopathogenesis of arthritis.",
author = "Kresina, {T. F.} and Jung Yoo and Goldberg, {V. M.}",
year = "1988",
language = "English (US)",
volume = "31",
pages = "248--257",
journal = "Arthritis and Rheumatology",
issn = "2326-5191",
publisher = "John Wiley and Sons Ltd",
number = "2",

}

TY - JOUR

T1 - Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology

AU - Kresina, T. F.

AU - Yoo, Jung

AU - Goldberg, V. M.

PY - 1988

Y1 - 1988

N2 - We examined antiproteoglycan antibodies as an autoimmune response for induction of synovitis. This hypothesis was studied by monitoring humoral antiproteoglycan antibody following IgG induction of experimental immuno synovitis, localization in the articular cartilage of an autologous immune response, and loss of proteoglycan from cartilage following intravenous administration of antiproteoglycan monoclonal antibodies. The data support the hypothesis that autoimmunity to cartilage macromolecules may play a role in the etiopathogenesis of arthritis.

AB - We examined antiproteoglycan antibodies as an autoimmune response for induction of synovitis. This hypothesis was studied by monitoring humoral antiproteoglycan antibody following IgG induction of experimental immuno synovitis, localization in the articular cartilage of an autologous immune response, and loss of proteoglycan from cartilage following intravenous administration of antiproteoglycan monoclonal antibodies. The data support the hypothesis that autoimmunity to cartilage macromolecules may play a role in the etiopathogenesis of arthritis.

UR - http://www.scopus.com/inward/record.url?scp=0023860761&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023860761&partnerID=8YFLogxK

M3 - Article

C2 - 3279964

AN - SCOPUS:0023860761

VL - 31

SP - 248

EP - 257

JO - Arthritis and Rheumatology

JF - Arthritis and Rheumatology

SN - 2326-5191

IS - 2

ER -