Oxygen free radicals denature human IgG and increase its reactivity with rheumatoid factor antibody

Joseph Lunec, Helen R. Griffiths, S. Brailsford

Research output: Contribution to journalArticle

Abstract

Rheumatoid inflammation is characterised by the production of rheumatoid factor antibodies directed against denatured IgG. Oxygen free radicals have the potential to denature all manner of proteins and can be generated by activated phagocytic cells in the inflamed joint. By modifying routine ELISA and nephelometric procedures for measuring rheumatoid factor, (i.e. substituting free radical altered IgG for rabbit and heat aggregated IgG as antigens) we have observed that oxygen radicals, generated by (1) UV light and (2) PMA-activated neutrophils, give rise to monomeric and polymeric forms of IgG which have increased reactivity towards IgM and IgA polyclonal rheumatoid factor antibodies. We conclude that free radical alteration of IgG may be a stimulus to the formation of immune complexes with rheumatoid factor antibody, thereby promoting and amplifying tissue damage during rheumatoid inflammation.
Original languageEnglish
Pages (from-to)140-7
Number of pages8
JournalScandinavian Journal of Rheumatology
Volume75
Issue numberSupplement
Publication statusPublished - 1988

Fingerprint

Rheumatoid Factor
Free Radicals
Reactive Oxygen Species
Immunoglobulin G
Antibodies
Inflammation
Ultraviolet Rays
Phagocytes
Antigen-Antibody Complex
Immunoglobulin A
Immunoglobulin M
Neutrophils
Hot Temperature
Joints
Enzyme-Linked Immunosorbent Assay
Rabbits
Antigens
Proteins

Keywords

  • Rheumatoid inflammation
  • free radical
  • denaturing protein
  • protein
  • activated phagocytic cell
  • antibody
  • tissue damage

Cite this

Lunec, Joseph ; Griffiths, Helen R. ; Brailsford, S. / Oxygen free radicals denature human IgG and increase its reactivity with rheumatoid factor antibody. In: Scandinavian Journal of Rheumatology. 1988 ; Vol. 75, No. Supplement. pp. 140-7.
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Oxygen free radicals denature human IgG and increase its reactivity with rheumatoid factor antibody. / Lunec, Joseph; Griffiths, Helen R.; Brailsford, S.

In: Scandinavian Journal of Rheumatology, Vol. 75, No. Supplement, 1988, p. 140-7.

Research output: Contribution to journalArticle

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AU - Lunec, Joseph

AU - Griffiths, Helen R.

AU - Brailsford, S.

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N2 - Rheumatoid inflammation is characterised by the production of rheumatoid factor antibodies directed against denatured IgG. Oxygen free radicals have the potential to denature all manner of proteins and can be generated by activated phagocytic cells in the inflamed joint. By modifying routine ELISA and nephelometric procedures for measuring rheumatoid factor, (i.e. substituting free radical altered IgG for rabbit and heat aggregated IgG as antigens) we have observed that oxygen radicals, generated by (1) UV light and (2) PMA-activated neutrophils, give rise to monomeric and polymeric forms of IgG which have increased reactivity towards IgM and IgA polyclonal rheumatoid factor antibodies. We conclude that free radical alteration of IgG may be a stimulus to the formation of immune complexes with rheumatoid factor antibody, thereby promoting and amplifying tissue damage during rheumatoid inflammation.

AB - Rheumatoid inflammation is characterised by the production of rheumatoid factor antibodies directed against denatured IgG. Oxygen free radicals have the potential to denature all manner of proteins and can be generated by activated phagocytic cells in the inflamed joint. By modifying routine ELISA and nephelometric procedures for measuring rheumatoid factor, (i.e. substituting free radical altered IgG for rabbit and heat aggregated IgG as antigens) we have observed that oxygen radicals, generated by (1) UV light and (2) PMA-activated neutrophils, give rise to monomeric and polymeric forms of IgG which have increased reactivity towards IgM and IgA polyclonal rheumatoid factor antibodies. We conclude that free radical alteration of IgG may be a stimulus to the formation of immune complexes with rheumatoid factor antibody, thereby promoting and amplifying tissue damage during rheumatoid inflammation.

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