T lymphocytes with low or absent expression of TCRzeta chain (TCR zeta -/dim cells) are supposed to have pathogenic effect in the developement of autoagression and chronic inflammation. Systemic lupus erythematosus (SLE) is a model of chronic inflammatory disease with autoimmune background.
In vitro studies have shown, that microenvironement rich in proinflammatory cytokines, such as TNF-alfa and IL-6, especially promotes the impairment of TCR zeta chain expression, what leads to the increase of the percentage of T cells with defects of the synthesis of that molecule.
Objective The aim of this study was to define the size of the population of autoreactive TCR zeta -/dim lymphocytes in the blood of patients with SLE and the functional characteristics of TCR zeta-/dim and TCR zeta bright cells based on the assessment of their capacity to synthetize certain cytokines (IFN-gamma and IL-2) and to compare it with healthy controls.
Results Our study showed decreased percentage of CD4 +and CD8+lymphocytes with TCR zeta chain expression in patients with SLE. The significantly diminished TCRzeta chain expression in lymphocytes of patients with SLE which in addition was correlated with longer disease duration, renal involvement and higher level of serum anti-dsDNA antibodies confirms former studies indicating not only the association of this defect with disease developement, but also with more active clinical course.
The in vitro stimulation of T lymphocytes in SLE patients lead to overproduction of IFN-gamma especially in the population of autoreactive TCR zeta -/dim lymphocytes.
On the other hand, T lymphocytes of SLE patients have lower capacity of the synthesis of IL-2, which is strongly correlated with TCR zeta chain expression and may be observed even in patients with very low clinical disease activity.
Conclusion SLE is characterised by the expanssion of TCR zeta -/dim lymphocytes in peripheral blood, which are regarded as autoreactive cells, and is correlated with clinical course of SLE. The decreased expression of TCR zeta may be due to the presence of exogenous inhibiting factor in blood of SLE patients. Higher synthesis of INF-gamma and lower of IL-2 may contribute to chronic inflammation and autoimmune proces in SLE.
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