Post-Stroke Immunodeficiency: Effects of Sensitization and Tolerization to Brain Antigens

Abstract

Acute onset of cerebrovascular diseases seems to be related to a number of immunological alternations. After the initial pro-inflammatory response to brain ischemia accompanied by systemic inflammatory response syndrome, stroke interferes with function of the innate and the adaptive immune cells, resulting in systemic immunosuppression. Although post-stroke immunodeficiency could predispose patients to life-threatening infections, it could potentially protect brain via reducing autoimmune reaction to the brain antigens. In this paper, we review current knowledge on the immunological alterations after brain ischemia, particularly effects of infection for stimulation of autoimmune response against brain antigens.

Effect of Yi-nao-jie-yu decoction on γ-aminobutyric acid type A receptor in the hippocampus and serum inflammatory factors in a rat model of poststroke anxiety

“…Brain injury occurs by initiation of localized and systemic inflammation responses. Accordingly, the influx of leukocytes into brain tissue increases brain inflammation via activation of cytokines, such as ILs and TNF 30. Serum levels of proinflammatory cytokines increase after brain ischemia and correlate with a worsened outcome 31.…”

Acute splenic responses in patients with ischemic stroke and intracerebral hemorrhage

“…7,31 The intricate pathways of immune system activation lead to a depressive state of peripheral immunity, the so-called post-stroke immunosuppression or post-stroke immunodeficiency. 3,32,33 A strong correlation between post-stroke activation of the immune system and changes in spleen have been described in animal models. 4 These include a reduction in number and apoptotic cell death of splenocytes, changes in cellularity and phenotype of splenocytes, and splenic atrophy.…”

Blood/Brain Biomarkers of Inflammation After Stroke and Their Association With Outcome: From C-Reactive Protein to Damage-Associated Molecular Patterns

“…In addition, the excessive concentration of proinflammatory mediators can promote the release of glucocorticoids and catecholamines by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. This results in the stimulation of anti-inflammatory pathways and the inhibition of proinflammatory mechanisms [14]. The rapid and inappropriate activation of these mechanisms also contributes to stroke-related immunosuppression, which enhances the risk of infection after cerebral ischemia.…”