Obeagu Emmanuel Ifeanyi
Department of Medical Laboratory Science, Kampala International University, Kampala, Uganda.
Ann Med Surg (Lond). 2024 Apr 3;86(5):2873-2882. doi: 10.1097/MS9.0000000000002019. eCollection 2024 May.
Malaria remains a significant global health challenge, demanding a deeper understanding of host immune responses for effective clearance of the parasitic infection. Cytokines, as crucial mediators of the immune system, orchestrate a complex interplay during the various stages of malaria infection. Throughout the course of the disease, an intricate balance of pro-inflammatory and anti-inflammatory cytokines dictate the immune response's outcome, influencing parasitic clearance and disease severity. During the initial stages, interleukins such as interleukin-12 (IL-12), interferon-gamma (IFN-γ), and tumour necrosis factor-alpha (TNF-α) play pivotal roles in activating innate immune cells, initiating the anti-parasitic response. Simultaneously, regulatory cytokines like interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β) modulate this immune activation, preventing excessive inflammation and tissue damage. As the infection progresses, a delicate shift occurs, characterized by a transition to adaptive immunity, guided by cytokines like interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13), promoting antibody production and T-cell responses. Notably, the resolution of malaria infection crucially relies on a fine-tuned balance of cytokine networks. Dysregulation or imbalances in these mediators often result in immune hyperactivation, contributing to severe manifestations and prolonged infection. Understanding the multi-faceted roles of cytokines in malaria clearance offers promising avenues for therapeutic interventions. Targeting cytokine pathways to restore immune equilibrium or bolster protective responses could potentially enhance treatment strategies and vaccine development. In conclusion, the pivotal role of cytokines in immunomodulation during malaria clearance underscores their significance as potential targets for therapeutic interventions, offering promising prospects in the global fight against this infectious disease.
疟疾仍然是一项重大的全球健康挑战,需要更深入地了解宿主免疫反应以有效清除寄生虫感染。细胞因子作为免疫系统的关键介质,在疟疾感染的各个阶段协调着复杂的相互作用。在疾病过程中,促炎细胞因子和抗炎细胞因子之间的微妙平衡决定了免疫反应的结果,影响着寄生虫的清除和疾病的严重程度。在初始阶段,白细胞介素-12(IL-12)、干扰素-γ(IFN-γ)和肿瘤坏死因子-α(TNF-α)等白细胞介素在激活先天免疫细胞、启动抗寄生虫反应中起关键作用。同时,白细胞介素-10(IL-10)和转化生长因子-β(TGF-β)等调节性细胞因子调节这种免疫激活,防止过度炎症和组织损伤。随着感染的进展,会发生微妙的转变,其特征是向适应性免疫过渡,由白细胞介素-4(IL-4)、白细胞介素-5(IL-5)和白细胞介素-13(IL-13)等细胞因子引导,促进抗体产生和T细胞反应。值得注意的是,疟疾感染的消退关键依赖于细胞因子网络的精细平衡。这些介质的失调或失衡通常会导致免疫过度激活,导致严重症状和感染延长。了解细胞因子在疟疾清除中的多方面作用为治疗干预提供了有希望的途径。靶向细胞因子途径以恢复免疫平衡或增强保护性反应可能会增强治疗策略和疫苗开发。总之,细胞因子在疟疾清除过程中的免疫调节中的关键作用突出了它们作为治疗干预潜在靶点的重要性,为全球抗击这种传染病提供了有希望的前景。