CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Tumor-infiltrating and circulating B cells mediate local and systemic immunomodulatory mechanisms in Glioblastoma.
Tumor-infiltrating and circulating B cells mediate local and systemic immunomodulatory mechanisms in Glioblastoma.
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了解 B 细胞的作用、它们如何被招募以及其分化如何转向免疫调节角色,可以为更好的治疗策略提供信息,并释放它们在 GBM 中的全部抗肿瘤潜力。
胶质母细胞瘤(GBM)表现出广泛的免疫调节机制,对有效的治疗干预构成挑战。这些现象远远超出肿瘤微环境(TME)的范围,并反映在循环免疫表型中。尽管B淋巴细胞(B细胞)在介导局部和全身免疫反应中的重要性日益显现,但在GBM研究中受到的关注有限。近期研究结果突显了B细胞与其他免疫细胞群体之间复杂的调控相互作用,包括肿瘤浸润巨噬细胞(TAMs)、髓源性抑制细胞(MDSCs)和其他浸润淋巴细胞(TILs)。B细胞被认为会阻碍以T细胞为重点的现代免疫治疗策略的疗效。
这是一篇聚焦于截至2025年1月关于GBM中B细胞现有证据的综述。
外周血反映出全身性免疫反应减弱,表现为持续性淋巴细胞减少、浆细胞增多以及记忆B细胞功能障碍。肿瘤免疫微环境中B系细胞富集。一些特征尚不明确的B调节细胞(Bregs)亚群存在于TME中,其表型的形成与靠近MDSCs、TAMs和肿瘤细胞有关。Bregs抑制CD8+ T细胞活性,可能具有潜在的预后意义。
Glioblastoma (GBM) demonstrates extensive immunomodulatory mechanisms that challenge effective therapeutic interventions. These phenomena extend well beyond the tumor microenvironment (TME) and are reflected in the circulating immunophenotype. B lymphocytes (B cells) have received limited attention in GBM studies despite their emerging importance in mediating both local and systemic immune responses. Recent findings highlight the complex regulatory interactions between B cells and other immune cell populations, including tumor-infiltrating macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), and other infiltrating lymphocytes (TILs). B cells are believed to hinder the efficacy of modern immunotherapy strategies focusing on T cells.
This is a focused review of available evidence regarding B cells in GBM through January 2025.
Peripheral blood reflects a systemically dampened immune response, with sustained lymphopenia, increased plasma cells, and dysfunctional memory B cells. The tumor immune landscape is enriched in cells of B-lineage. Subsets of poorly characterized B regulatory cells (Bregs) populate the TME, developing their phenotype due to their proximity to MDSCs, TAMs, and tumoral cells. The Bregs inhibit CD8 + T activity and may have potential prognostic significance.
Understanding the role of B cells, how they are recruited, and their differentiation shifted towards an immunomodulatory role could inform better therapeutic strategies and unleash their full antitumoral potential in GBM.
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