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Isolation of functional polyclonal TsF from MRL-lpr spleens using monoclonal antibody absorbance
Authors:J K Steele  A T Stammers  J G Levy  J D Waterfield
Institution:1. Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China;2. Maternal-Fetal Institute, Shenzhen Baoan Women''s and Children''s Hospital, Jinan University, Shenzhen, China;3. Department of Pediatrics, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China;4. Reproduction and Development, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China;5. School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China;6. Chinese University of Hong Kong-Sichuan University Joint Laboratory in Reproductive Medicine, The Chinese University of Hong Kong, Hong Kong, China;7. Maternal-Fetal Institute, Shenzhen Baoan Women''s and Children''s Hospital, Shenzhen University, Shenzhen, China;1. Oncoimmunology Research Unit, Navarrabiomed-Fundación Miguel Servet, Hospital Universitario de Navarra (HUN), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona, Spain;2. Division of Gene Therapy and Regulation of Gene Expression, Cima Universidad de Navarra and Instituto de Investigación Sanitaria de Navarra (IdISNA), Pamplona, Spain
Abstract:We have previously described a monoclonal antibody, B16G, which has been found to be specific for T-cell derived suppressor factors (TsF). B16G has been shown to react with T-suppressor cells, TsF in the spleens of normal or tumor-bearing mice, the TsF produced by a tumor-specific T-cell hybridoma, and with polyclonal whole human TsF isolated from tonsilar tissue. This panreactivity inherent to the B16G MAb has made it clear that it recognizes some common, shared epitope of the TsF molecule. In this study we have used B16G as a probe to isolate TsF from the spleens of MRL-lpr mice and compare the activity with these factors isolated from the spleens of an MHC compatible nonautoimmune strain, CBA. We find that equivalent quantities of functional TsF are isolable from both strains and thus, it can be concluded that the associated oligoclonal B-cell activation characteristic of MRL-lpr mice is not due to a polyclonal T-suppressor cell deficit, nor to the ability of TsC in these mice to produce soluble, functional TsFs. The molecular and biochemical characteristics of these TsFs are discussed.
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