Abstract
The immunology of stroke can be approached in several ways. By viewing stroke from an immunological standpoint, we are trying to achieve new insights in its pathogenesis and reach new therapeutic options. To review and summarize the findings from publications on immunology of stroke. Infections are a well-known risk factor for stroke. This is due to activated immune cells interacting with throm-bocytes and releasing coagulation factors, which affect the formation of the thrombus. Aseptic inflammation in the ischemic lesion leads to cellular invasion of the area and triggers a pro-inflammatory response, which has an impact on further destruction of ischemic brain tissue. Another aspect of stroke is systemic immune suppression, which is a predisposing factor towards a systemic bacterial infection. Infection itself is also an independent risk factor for negative clinical outcomes and increased mortality. The immunological approach to the topic of ischemic stroke holds significant value for future research.
Highlights
Immune response and inflammation are key elements in the pathobiology of ischemic stroke
While immunity contributes to brain damage due to ischemia, the damaged tissue itself triggers a powerful immunosuppressive response, which in turn leads to potentially life-threatening intercurrent infections
It is important to keep in mind that immunomodulation can lead to some serious side effects and continuously studying the connections between immunity and ischemic brain damage is essential
Summary
Immune response and inflammation are key elements in the pathobiology of ischemic stroke. This large-scale trial failed to prove a significant difference in outcome between patients given minocycline and patients given placebo Another therapeutic approach is blocking neutrophil activity using a recombinant neutrophil-inhibiting factor.[23] This molecule demonstrates a reduction in neutrophil infiltration and lesion volume in animal models. The patients were aged 18-80 years, had a NIHSS>5, no contraindications for thrombolysis, no dysphagia, did not take any other cytostatic or immunosuppressive medication In this trial, there was a decreased number of circulating lymphocytes, a smaller lesion volume (10.1 ml compared to 34.3 ml; p=0.04), fewer hemorrhagic complications and a lower NIHSS score (4 vs 2; p=0.02) on the first day. This reduction in the number of circulating lymphocytes seems to be the main difference between the effect of fingolimod and natalizumab on stroke patients and at this time it can be inferred that it plays a major part in the differing effects of their usage in stroke patients
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