OBJECTIVE: To study the immunological consequences of systemic thalidomide treatment in patients with Sjögren's syndrome. METHODS:Cytokine (tumour necrosis factor alpha (TNFalpha), interleukin (IL) 6) and soluble receptor (sIL2R) levels were measured in patient and control plasma (n = 7), before and after thalidomide treatment. Peripheral blood mononuclear cells were examined by FACS analysis for potential changes in specific cell populations (T cells, B cells, monocytes), and for the expression of activation markers (CD25, HLA-DR), costimulatory molecules (CD40, CD40L), TNF receptors, chemokine receptors, and adhesion molecules (L-selectin (L-sel)). RESULTS: Owing to adverse effects of thalidomide, the treatment interval was limited. None the less, statistically significant changes in markers of cell activation were recorded in the four treated patients. Before treatment, HLA-DR, TNFRI, CXCRI, and CXCRII were raised in the patients compared with healthy controls (p<0.05) and their expression was down regulated after treatment. B cell numbers and expression of the adhesion molecule L-sel also declined with thalidomide. CONCLUSION: Significant changes in measures of cell activation were detected during thalidomide treatment within this limited study, which upon further investigation may offer insight into the underlying immunoregulatory pathways of thalidomide.
RCT Entities:
OBJECTIVE: To study the immunological consequences of systemic thalidomide treatment in patients with Sjögren's syndrome. METHODS: Cytokine (tumour necrosis factor alpha (TNFalpha), interleukin (IL) 6) and soluble receptor (sIL2R) levels were measured in patient and control plasma (n = 7), before and after thalidomide treatment. Peripheral blood mononuclear cells were examined by FACS analysis for potential changes in specific cell populations (T cells, B cells, monocytes), and for the expression of activation markers (CD25, HLA-DR), costimulatory molecules (CD40, CD40L), TNF receptors, chemokine receptors, and adhesion molecules (L-selectin (L-sel)). RESULTS: Owing to adverse effects of thalidomide, the treatment interval was limited. None the less, statistically significant changes in markers of cell activation were recorded in the four treated patients. Before treatment, HLA-DR, TNFRI, CXCRI, and CXCRII were raised in the patients compared with healthy controls (p<0.05) and their expression was down regulated after treatment. B cell numbers and expression of the adhesion molecule L-sel also declined with thalidomide. CONCLUSION: Significant changes in measures of cell activation were detected during thalidomide treatment within this limited study, which upon further investigation may offer insight into the underlying immunoregulatory pathways of thalidomide.
Authors: C Vitali; S Bombardieri; R Jonsson; H M Moutsopoulos; E L Alexander; S E Carsons; T E Daniels; P C Fox; R I Fox; S S Kassan; S R Pillemer; N Talal; M H Weisman Journal: Ann Rheum Dis Date: 2002-06 Impact factor: 19.103
Authors: Stanley R Pillemer; Rose Anne Leakan; Vidya Sankar; Joan Manny; Bruce J Baum; Janine Smith; Usha Chaudhry; Philip C Fox; Lida Radfar; Sophie Ligier; Michael T Brennan Journal: Arthritis Rheum Date: 2004-06-15
Authors: J M Jacobson; J S Greenspan; J Spritzler; N Ketter; J L Fahey; J B Jackson; L Fox; M Chernoff; A W Wu; L A MacPhail; G J Vasquez; D A Wohl Journal: N Engl J Med Date: 1997-05-22 Impact factor: 91.245
Authors: Clio P Mavragani; Timothy B Niewold; Niki M Moutsopoulos; Stanley R Pillemer; Sharon M Wahl; Mary K Crow Journal: Arthritis Rheum Date: 2007-12
Authors: Gikas E Katsifis; Sofia Rekka; Niki M Moutsopoulos; Stanley Pillemer; Sharon M Wahl Journal: Am J Pathol Date: 2009-08-21 Impact factor: 4.307