TY - JOUR
T1 - Immunological consequences of thalidomide treatment in Sjögren's syndrome
AU - Moutsopoulos, N. M.
AU - Angelov, N.
AU - Sankar, V.
AU - Leakan, R. A.
AU - Pillemer, S.
AU - Wahl, S. M.
PY - 2006/1
Y1 - 2006/1
N2 - Objective: To study the immunological consequences of systemic thalidomide treatment in patients with Sjögren's syndrome. Methods: Cytokine (tumour necrosis factor α (TNFα), interleukin (IL) 6) and soluble receptor (slL2R) 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.
AB - Objective: To study the immunological consequences of systemic thalidomide treatment in patients with Sjögren's syndrome. Methods: Cytokine (tumour necrosis factor α (TNFα), interleukin (IL) 6) and soluble receptor (slL2R) 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.
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U2 - 10.1136/ard.2005.038406
DO - 10.1136/ard.2005.038406
M3 - Article
C2 - 16344495
AN - SCOPUS:29144466435
VL - 65
SP - 112
EP - 114
JO - Annals of the Rheumatic Diseases
JF - Annals of the Rheumatic Diseases
SN - 0003-4967
IS - 1
ER -