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The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?

Systemic lupus erythematosus, considered a multifactorial autoimmune disease, is a disease affecting many systems, with associated immunological abnormalities. It has a striking diversity of clinical patterns, pathologies and prognoses. Genetic factors determine the inherited baseline, on which envi...

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Main Author: Yell, Jennifer Anne
Format: Thesis
Language:English
Published: Division of Dermatology 2017
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access_status_str Open Access
author Yell, Jennifer Anne
author_browse Yell, Jennifer Anne
author_facet Yell, Jennifer Anne
author_sort Yell, Jennifer Anne
collection Thesis
description Systemic lupus erythematosus, considered a multifactorial autoimmune disease, is a disease affecting many systems, with associated immunological abnormalities. It has a striking diversity of clinical patterns, pathologies and prognoses. Genetic factors determine the inherited baseline, on which environmental, hormonal and infectious triggers act to produce autoantibodies. Ro antibodies have been considered pathogenic in subacute cutaneous and neonatal lupus erythematosus. I affinity-purified antibodies to the 52 kD Ro from immunised rabbits (whole 52 kD protein) and human sera (using two immunodominant regions of the protein). I affinity-purified antibodies to the 60 kD Ro from immunised rabbits (whole 60 kD protein) and human sera (using two immunodominant regions of the protein, as well as the total "native" protein). Using these purified antibodies, with immunofluorescence on normal neonatal human keratinocytes, I showed that the 52 kD Ro is mainly cytoplasmic and the 60 kD Ro is mostly nuclear, with some fine cytoplasmic staining. I looked at the capacity of these purified antibodies to penetrate living keratinocytes under various conditions (hormones, drugs and vitamins). No antibody penetration was found, although one whole serum gave low levels of intracellular fluorescence. I studied the putative membrane translocation of 52 kD and 60 kD Ro under conditions of stress (UV A or UVB with or without hormones, drugs, vitamins and heat shock). I could not identify translocation of the 52 or 60 kD antigens with purified antibodies, although some whole sera showed fluorescence. I can find no evidence that antibodies directed against the 52 and 60 kD Ro antigens cause cutaneous disease.
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institution University of Cape Town (South Africa)
language eng
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provenance_str_mv Harvested via OAI-PMH from UCTD — University of Cape Town Open Access Repository
publishDate 2017
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spelling oai:open.uct.ac.za:11427/25683 The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease? Yell, Jennifer Anne Dermatology Systemic lupus erythematosus, considered a multifactorial autoimmune disease, is a disease affecting many systems, with associated immunological abnormalities. It has a striking diversity of clinical patterns, pathologies and prognoses. Genetic factors determine the inherited baseline, on which environmental, hormonal and infectious triggers act to produce autoantibodies. Ro antibodies have been considered pathogenic in subacute cutaneous and neonatal lupus erythematosus. I affinity-purified antibodies to the 52 kD Ro from immunised rabbits (whole 52 kD protein) and human sera (using two immunodominant regions of the protein). I affinity-purified antibodies to the 60 kD Ro from immunised rabbits (whole 60 kD protein) and human sera (using two immunodominant regions of the protein, as well as the total "native" protein). Using these purified antibodies, with immunofluorescence on normal neonatal human keratinocytes, I showed that the 52 kD Ro is mainly cytoplasmic and the 60 kD Ro is mostly nuclear, with some fine cytoplasmic staining. I looked at the capacity of these purified antibodies to penetrate living keratinocytes under various conditions (hormones, drugs and vitamins). No antibody penetration was found, although one whole serum gave low levels of intracellular fluorescence. I studied the putative membrane translocation of 52 kD and 60 kD Ro under conditions of stress (UV A or UVB with or without hormones, drugs, vitamins and heat shock). I could not identify translocation of the 52 or 60 kD antigens with purified antibodies, although some whole sera showed fluorescence. I can find no evidence that antibodies directed against the 52 and 60 kD Ro antigens cause cutaneous disease. 2017-10-16T10:27:32Z 2017-10-16T10:27:32Z 1998 2017-07-19T14:18:09Z Doctoral Thesis Doctoral MD http://hdl.handle.net/11427/25683 eng application/pdf Division of Dermatology Faculty of Health Sciences University of Cape Town
spellingShingle Dermatology
Yell, Jennifer Anne
The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?
thesis_degree_str Doctoral
title The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?
title_full The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?
title_fullStr The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?
title_full_unstemmed The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?
title_short The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?
title_sort 52 and 60 kd ro ss a antigens where are they do anti ro ss a autoantibodies cause cutaneous disease
topic Dermatology
url http://hdl.handle.net/11427/25683
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