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AB0023 in vitro peripheral blood mononuclear cells autoreactivity against autologous epidermal cells and the presence of anti-skin autoantibodies in patients with rheumatoid arthritis
  1. IJ Hromadnikova,
  2. P Vavrincova,
  3. K Stechova,
  4. M Cermakova-Frantlova,
  5. D Chudoba,
  6. J Vavrinec
  1. 2Nd Paediatric Clinic, University Hospital Motol, Prague 5, Czech Republic

Abstract

Background We discuss the ability of peripheral blood mononuclear cells (PBMN) of patients with rheumatoid arthritis (RA) or juvenile idiopathic arthritis to damage autologous skin or lyse autologous keratinocytes if co-cultured in vitro.

We discuss a well as the presence of anti-skin anti-intercellular (ASA-IC), anti-skin anti-basement membrane (ASA-BM) and anti-keratin (AKA) antibodies of IgG class in patients´ sera without clinical features of vesicular bullous diseases.

Methods A modified in vitro skin explant assay originally developed to predict acute graft versus host disease (GvHD) in allogeneic stem cell transplants was used in order to see if GvHR-like histopathological changes occur when patients´ PMNC would be co-cultured with autologous skin. 51Cr release cytotoxic assay was used to prove if observed skin damage was really of an autoimmune origin. An indirect immunofluorescence test on rat, monkey and guinea pig oesophagus substrates was used for the detection and quantification of ASA-IC, ASA-BM and AKA antibodies.

Results We found out that PBMN of 29 out of 34 patients with RA or JIA (85,3%) were able to induce histopathological changes of grade II or above in autologous skin explants. Similarly, we observed that PBMN lysed autologous keratinocytes, but not autologous lymphoblasts when co-cultured in vitro.

No skin damage or keratinocytes lysis was observed in healthy controls. Overall ASA-IC were detected in 50 out of 57 studied patients´ sera samples (87,7%, p = 0,0003). No ASA-BM  positivity was observed in a studied cohort. AKA were detectable in 33 out of 60 patients (55%, p = 0,0001).

Conclusion We suggest that PBMN of patients with RA or JIA might recognise similar autoantigen (s) expressed on epidermal cells that give rise an autoimmune response in synovium. However we observed a high incidence of ASA-IC antibodies in patients with RA and JIA we suppose that subclinical pemphigus occurring in this group might be exacerbated with different stimulus including pemphigus inducing drugs.

References

  1. Osteolog Bull. 2000;2:70–11

  2. Czech Rheumatol. 1999;4:166–74

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