An FcγRIII (CD16)-specific autoantibody from a patient with progressive systemic sclerosis

Andrea Szegedi, Peter Boros, Jiayuan Chen, Martin Kaffina, Constantin Bona, Jay C. Unkeless

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Polyspecific and organ specific autoimmune diseases are often accompanied by prolonged clearance of immune complexes. In mice, impaired macrophage Fcγ receptor function may be associated with autoantibody against Fcγ receptors. To extend these observations to autoimmune human disease, we transformed with EBV peripheral lymphocytes from a patient with terminal progressive systemic sclerosis and screened for clones secreting anti-Fcγ receptor Ig. A clone, N55, which secretes a high affinity anti-Fcγ receptor IgG2 antibody was obtained. The Fab fragment of N55 bound to human neutrophils, NK cells, but not to monocytes, consistent with specificity for FcγRIII (CD16). N55 Fab competed weakly for the binding of anti-FcγRIII mAb 3G8 to neutrophils but did not have any effect on staining with the anti-FcγRII mAb, IV.3. N55 Fab did not bind to peripheral monocytes, but did bind to monocytes incubated with TGF-β (24 h) to induce FcγRIII. The specificity of N55 IgG for FcγRIII was confirmed by ELISA using secreted recombinant FcγRIIA and FcγRIIIB protein to coat microtiter wells. N55 IgG triggered the release from neutrophils of β-glucuronidase, arylsulfatase and alkaline phosphatase. Such antibody may play a pathogenic role in progressive systemic sclerosis.

Original languageEnglish
Pages (from-to)69-76
Number of pages8
JournalImmunology Letters
Volume35
Issue number1
DOIs
StatePublished - Jan 1993

Keywords

  • Autoantibodies
  • FcRIII (CD16)
  • Neutrophils
  • Progressive systemic sclerosis

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