骨髓纤维化（MF）主要是由于雄性激素激活素激酶（JAK）/信号传导调节因子（STAT）通路的持续激活所驱动。虽然JAK抑制剂已被证明可以减轻疾病症状，但它们在MF的疾病修饰效果有限。唯一的治愈性治疗仍然是异基因干细胞移植，这只适用于少数患者。因此，有必要在MF中探索新的目标，以促进适当的药物开发和治疗途径。最近的研究集中于识别有助于造血和间质细胞异常相互作用的新型信号，促进MF和疾病进展。炎症和免疫调节失常已经成为MF起始和进展的关键驱动因素。已经确定了越来越多的可行靶点，包括细胞因子、转录因子、信号网络和细胞表面相关分子。这些靶点不仅在恶性和非恶性造血细胞中显示功能失调，还在骨髓的非造血细胞中显示功能失调。对这些与炎症相关的分子在临床前模型和MF患者样本中的研究，为提供新的治疗靶点提供了基础。免疫治疗靶点的鉴定正在扩大MF的治疗领域。本综述总结了MF中免疫治疗靶点研究的最新进展。版权所有 © 2023 Wolters Kluwer Health, Inc. 保留所有权利。

Myelofibrosis (MF) is primarily driven by constitutive activation of the Janus kinase/signal transducer of activators of transcription (JAK/STAT) pathway. While JAK inhibitors have shown to alleviate disease symptoms, their disease-modifying effects in MF are limited. The only curative treatment remains allogeneic stem cell transplantation, which can be applied to a minority of patients. As a result, there is a need to explore novel targets in MF to facilitate appropriate drug development and therapeutic pathways.Recent research has focused on identifying novel signals that contribute to the abnormal cross-talk between hematopoietic and stromal cells, which promotes MF and disease progression. Inflammation and immune dysregulation have emerged as key drivers of both the initiation and progression of MF. A growing number of actionable targets has been identified, including cytokines, transcription factors, signalling networks and cell surface-associated molecules. These targets exhibit dysfunctions in malignant and nonmalignant hematopoietic cells, but also in nonhematopoietic cells of the bone marrow. The study of these inflammation-related molecules, in preclinical models and MF patient's samples, is providing novel therapeutic targets.The identification of immunotherapeutic targets is expanding the therapeutic landscape of MF. This review provides a summary of the most recent advancements in the study of immunotherapeutic targets in MF.Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.