scholarly journals Autoantigen-specific T cell proliferation induced by the ribosomal P2 protein in patients with systemic lupus erythematosus.

1994 ◽  
Vol 94 (1) ◽  
pp. 345-352 ◽  
Author(s):  
M K Crow ◽  
G DelGiudice-Asch ◽  
J B Zehetbauer ◽  
J L Lawson ◽  
N Brot ◽  
...  
1981 ◽  
Vol 153 (6) ◽  
pp. 1405-1414 ◽  
Author(s):  
A N Theofilopoulos ◽  
R S Balderas ◽  
D L Shawler ◽  
S Lee ◽  
F J Dixon

In young adulthood, MRL/Mp-lpr/lpr mice develop severe systemic lupus erythematosus (SLE)-like syndrome associated with massive T cell proliferation. The congenic MRL/Mp- mice lack the lpr gene and develop chronic SLE late in life. We have exchanged thymic transplants between these substrains so as to determine the role of the thymus in the development of early, severe SLE and of lymphoproliferation. The median survival times of unmanipulated lpr/lpr and mice were 160 and 510 d, respectively. The lpr/lpr and mice thymectomized when newborn and transplanted at 1 mo with the opposite type of thymus retained the diseases phenotype of their unmanipulated counterparts with 50% mortality at 186 and 498 d, respectively. In contrast, lpr/lpr mice thymectomized when newborn but not transplanted with thymus did not develop lymphoid hyperplasia and glomerulonephritis, and 100% of them were alive at 390 d. Serologically, the thymectomized but untransplanted lpr/lpr mice had significantly reduced levels of autoantibodies, whereas thymectomized and transplanted mice of either substrain were similar to unmanipulated controls. The results indicate that: (a) a thymus is essential for expression of lymphoproliferation and early SLE-like disease in the lpr/lpr phenotype; (b) the lpr/lpr disease is not a result of a unique hormonal or microenvironmental defect(s) of the thymus of this substrain because the genotype of the thymus is irrelevant for the development of T cell proliferation and early SLE; (c) differentiation of stem cells under the hormonal or microenvironmental influences of a thymus that possesses the lpr genotype does not lead to abnormal T cell differentiation or early autoimmunity; and (d) the lpr/lpr disease cannot be caused exclusively by an intrinsic B cell defect or environmental stimuli that cause B cell polyclonal activation.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Zhimin Lu ◽  
Dinglei Su ◽  
Dandan Wang ◽  
Xia Li ◽  
Xuebing Feng ◽  
...  

Objective. To investigate the frequency of peripheralγδT cells in patients with systemic lupus erythematosus (SLE) and its correlation with disease activity and to analyze the apoptotic status, proliferation ability, and intracellular cytokine profile of these cells.Methods. Flow cytometry was performed to detect the percentage and intracellular cytokine expression of peripheralγδT cells from SLE patients. Annexin-V/PI double staining was applied to determine the proportion of apoptoticγδand CD3+T cells.γδT cell proliferation was analyzed by CFSE labeling technique.Results. The percentage and absolute number ofγδT cells were remarkably decreased in active SLE patients compared to those in inactive patients and healthy controls, withγδT cell count negatively correlated with disease activity. Compared with healthy controls, peripheralγδT cells from active SLE patients exhibited higher apoptotic rate and lower proliferation ability, as well as elevated expression of intracellular IFN-γ, IL-4, IL-10, and TGF-β, but not IL-17 or Foxp3.Conclusion. DecreasedγδT cells in the peripheral blood of SLE patients might be caused by upregulated apoptosis and downregulated cell proliferation. TheseγδT cells may secret both pro- and anti-inflammatory cytokines to perform their functions in SLE.


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