iNKT细胞与缺血性脑卒中后免疫抑制关系的研究进展

Research progress on the relationship between iNKT cells and immunosuppression after ischemic stroke

摘要:

缺血性脑卒中即各种脑血管病变导致的脑组织供血供氧障碍从而出现的神经系统损伤。卒中后免疫抑制诱发的严重感染是影响患者生存预后的重要因素。抗生素治疗受到药物耐药性增加的限制，因此，免疫调节治疗受到广泛的关注。卒中后，不变的自然杀伤T细胞（iNKT）在免疫抑制中发挥重要作用，其作为上游调节免疫系统中的CD4⁺T和CD8⁺T细胞，促使免疫系统Th1向Th2改变，从而导致卒中后免疫抑制。用α-半乳糖神经酰胺（α-GalCer）直接调节iNKT细胞或通过阻断去甲肾上腺素能神经递质有助于减少卒中后的感染率。但iNKT细胞如何被远距离激活，如何在卒中后推动免疫系统改变的机制尚不明确。该文就iNKT细胞的生物学特征、功能及如何影响卒中后免疫抑制做一综述。

Abstract:

Ischemic stroke refers to the neurological damage caused by various cerebral vascular diseases. Severe infection induced by immunosuppression after stroke is an important factor affecting the survival and prognosis of patients. Although antibiotic therapy is effective to a certain extent, immunomodulatory therapy has received a lot of attention as drug resistance has increased. invariant Natural Killer T-cells (iNKT) play an important role in post-stroke immunosuppression, acting as upstream modulators of CD4⁺T and CD8⁺T Cells in the immune system to induce the changes from Th1 to Th2. Which leads to post-stroke immunosuppression. Regulating iNKT cells directly with alpha-galactoceramide (alpha-Galcer) or by blocking norepinephrinic neurotransmitters is known to help reduce infection rates after stroke. But the mechanism of how iNKT cells are activated at a distance and how they drive changes in the immune system after stroke has been unclear. This article reviews the biological characteristics, functions and effects of iNKT cells on post-stroke immunosuppression.