Defective monocyte function in patients with systemic lupus erythematosus |
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| Authors: | R Phillips R Lomnitzer A A Wadee A R Rabson |
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| Affiliation: | 1. Department of Cardiology, Rui Jin Hospital, Shanghai Jiaotong University School of Medicine, People''s Republic of China;2. Institute of Cardiovascular Diseases, Shanghai Jiaotong University School of Medicine, Shanghai 200025, People''s Republic of China;3. “G. d''Annunzio University”, Chieti, Italy;4. Fondazione “G. Monasterio”, Pisa, Italy;1. Department of Pharmacology & Toxicology, Michigan State University, United States;2. Department of Pathobiology & Diagnostic Investigation, Michigan State University, United States;3. Institute for Integrative Toxicology, Michigan State University, East Lansing, MI, United States;4. Surgical Research Laboratory, Department of Surgery, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands;1. Dept of Infection, Heartlands Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK;2. Public Health England, Heartlands Hospital, UK;3. Dept of Renal Medicine, Heartlands Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK;4. Institute of Applied Health Research, University of Birmingham, Birmingham, UK;5. Medical Innovation, Research and Development Unit, University Hospitals Birmingham Foundation Trust, Birmingham, UK;1. Department of Immunology, National Institute for Research in Tuberculosis (Formerly Tuberculosis Research Centre), Indian Council of Medical Research, 1, Mayor Sathyamoorthy Road, Chennai 600 031, India;2. HIV/AIDS Laboratory, Dept. of Clinical Research, National Institute for Research in Tuberculosis (Formerly Tuberculosis Research Centre), Indian Council of Medical Research, 1, Mayor Sathyamoorthy Road, Chennai 600 031, India |
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| Abstract: | Peripheral blood adherent cells from patients with systemic lupus erythematosus (SLE) were shown to have markedly reduced phagocytic activity as compared to normal adherent cells or those from non-SLE patients receiving corticosteroid therapy. Both resting and phagocytosing monocytes showed decreased hexose monophosphate shunt and glycolytic activity. Mononuclear cells from SLE patients showed grossly impaired proliferative activity after NaIO4 activation. Furthermore, addition of SLE adherent cells to normal adherent cell-depleted lymphocytes decreased [3H]thymidine incorporation of the latter cells following NaIO4 treatment. Addition of normal adherent cells to SLE lymphocytes corrected the previous defect, indicating that an adherent abnormality is responsible for the defect in SLE mononuclear cell proliferation to NaIO4 activation. |
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