[The relationship between immunological parameters with etiopathogenesis and clinical course of stroke]

We observed a lot of immune system disorders significantly influencing the development and clinical course of stroke. Depression of cell-mediated immune reactivity was observed in the early stage of stroke. It was manifested by the decrease of the number of T lymphocytes, depression in lymphocyte blastogenesis, diminished production of the migration inhibition factor and reduced delayed-type skin reactivity. Observed depression was probably caused by severe metabolic and endocrinological disorders often seen in the acute phase of the disease and related with increased patients' susceptibility to infections. Simultaneously we observed that the elevated total WBC was an independent stroke risk factor and predictor of 30-days stroke fatality. The activation of the adhesion molecules expression on granulocytes (CD18) and the increased cytokine production by leukocytes could favour leukocytes influence to the ischemic area and potentiate brain injury. The chronic inflammation could be also responsible for the development of vascular injuries leading to the ischemia. In our studies we demonstrated the high levels of antibodies to cardiolipins and heat shock proteins and the increased blood levels of immune complexes (i.c.). We observed the presence of Chlamydia pneumoniae and CMV antigens in isolated i.c. It suggests that different markers of chronic inflammation observed at very early stage of the disease are probably related with the chronic infection potentially leading to the development of atherosclerotic lesions and destabilization of atherosclerotic plaque.