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

dc.contributor.authorYell, Jennifer Anneen_ZA
dc.date.accessioned2017-10-16T10:27:32Z
dc.date.available2017-10-16T10:27:32Z
dc.date.issued1998en_ZA
dc.date.updated2017-07-19T14:18:09Z
dc.description.abstractSystemic 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.en_ZA
dc.identifier.apacitationYell, J. A. (1998). <i>The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?</i>. (Thesis). University of Cape Town ,Faculty of Health Sciences ,Division of Dermatology. Retrieved from http://hdl.handle.net/11427/25683en_ZA
dc.identifier.chicagocitationYell, Jennifer Anne. <i>"The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?."</i> Thesis., University of Cape Town ,Faculty of Health Sciences ,Division of Dermatology, 1998. http://hdl.handle.net/11427/25683en_ZA
dc.identifier.citationYell, J. 1998. The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?. University of Cape Town.en_ZA
dc.identifier.ris TY - Thesis / Dissertation AU - Yell, Jennifer Anne AB - 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. DA - 1998 DB - OpenUCT DP - University of Cape Town LK - https://open.uct.ac.za PB - University of Cape Town PY - 1998 T1 - The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease? TI - The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease? UR - http://hdl.handle.net/11427/25683 ER - en_ZA
dc.identifier.urihttp://hdl.handle.net/11427/25683
dc.identifier.vancouvercitationYell JA. The 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?. [Thesis]. University of Cape Town ,Faculty of Health Sciences ,Division of Dermatology, 1998 [cited yyyy month dd]. Available from: http://hdl.handle.net/11427/25683en_ZA
dc.language.isoengen_ZA
dc.publisher.departmentDivision of Dermatologyen_ZA
dc.publisher.facultyFaculty of Health Sciencesen_ZA
dc.publisher.institutionUniversity of Cape Town
dc.subject.otherDermatologyen_ZA
dc.titleThe 52 and 60 kD Ro/SS-A : antigens where are they? : do anti-Ro/SS-A autoantibodies cause cutaneous disease?en_ZA
dc.typeDoctoral Thesis
dc.type.qualificationlevelDoctoral
dc.type.qualificationnameMDen_ZA
uct.type.filetype
uct.type.filetypeText
uct.type.filetypeImage
uct.type.publicationResearchen_ZA
uct.type.resourceThesisen_ZA
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