Subalakshmi Sugumar, Rushendran R, Vellapandian Chitra
Department of Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, Chengalpattu, Tamil Nadu, 603203, India.
J Neuroimmune Pharmacol. 2025 Apr 2;20(1):30. doi: 10.1007/s11481-025-10197-3.
Migraine is a prevalent neurological disorder characterized by severe, recurrent headaches accompanied by symptoms, such as nausea, photophobia, and phonophobia, significantly affecting the quality of life of millions of people worldwide. Although the neurovascular pathway, involving blood vessel dilation and neurogenic inflammation, has been a cornerstone in understanding migraine pathophysiology. Emerging evidence suggests that immune dysregulation plays a pivotal role in the onset and progression of migraine. This review uniquely synthesizes recent advances linking immune regulatory pathways to migraine, an area that has not been widely explored in the literature. Specifically, we highlighted the involvement of CD4 + CD25 + regulatory T (Treg) cells, interleukins, and pro-inflammatory and anti-inflammatory cytokines, which have been implicated in pain signaling and immune imbalance in patients with migraine. Furthermore, genetic studies have provided compelling evidence by identifying associations between migraine susceptibility and immune-related polymorphisms, particularly in forkhead box P3 (FOXP3) and nuclear factor of activated T cells (NFAT). Moreover, the higher prevalence of migraine in individuals with comorbid autoimmune diseases further supports the hypothesis of a shared pathophysiological mechanism. Despite the growing recognition of immune involvement in migraine, its precise mechanisms remain unclear. By integrating key immune biomarkers and genetic insights, this review proposes a novel framework for understanding the immune-mediated pathways in migraine progression. Future research should focus on elucidating the specific immunological mechanisms underlying migraine, which could open new avenues for innovative, targeted therapeutic strategies.
偏头痛是一种常见的神经系统疾病，其特征为严重的复发性头痛，并伴有恶心、畏光和畏声等症状，严重影响全球数百万人的生活质量。尽管涉及血管扩张和神经源性炎症的神经血管途径一直是理解偏头痛病理生理学的基石，但新出现的证据表明免疫失调在偏头痛的发作和进展中起关键作用。本综述独特地综合了将免疫调节途径与偏头痛联系起来的最新进展，这一领域在文献中尚未得到广泛探索。具体而言，我们强调了CD4 + CD25 +调节性T（Treg）细胞、白细胞介素以及促炎和抗炎细胞因子的参与，这些细胞因子与偏头痛患者的疼痛信号传导和免疫失衡有关。此外，遗传学研究通过确定偏头痛易感性与免疫相关多态性之间的关联，特别是在叉头框P3（FOXP3）和活化T细胞核因子（NFAT）方面，提供了令人信服的证据。此外，自身免疫性疾病合并症患者中偏头痛的患病率较高，进一步支持了共同病理生理机制的假设。尽管人们越来越认识到免疫在偏头痛中的作用，但其确切机制仍不清楚。通过整合关键的免疫生物标志物和遗传学见解，本综述提出了一个理解偏头痛进展中免疫介导途径的新框架。未来的研究应专注于阐明偏头痛背后的具体免疫机制，这可能为创新的靶向治疗策略开辟新途径。
