Page 137 - 南京医科大学自然版

第46卷第9期 孟明辉，陈正新，王慧博. 翻译后修饰介导的膜表面稳态调控与胶质母细胞瘤免疫可见性重塑［J］.
2026年9月 南京医科大学学报（自然科学版），2026，46（9）：1398-1411 ·1407 ·

表3 GBM免疫可见性相关膜表面稳态调控机制的证据等级与适用边界
Table 3 Evidence levels and applicability boundaries of membrane surface homeostasis mechanisms related to immune visi⁃
bility in GBM

Mechanism/Axis Immune visibility role Representative GBM evidence Level Key limitation
PD ⁃ L1 regula⁃ Adaptive immune sup⁃ GBM⁃related evidence links PD⁃L1 to GSC B/C Most PTM mechanisms are extrapo⁃
tion pression states，β⁃catenin signaling and EV lated from other tumors

EV⁃PD⁃L1 out⁃ Distributed adaptive IFN⁃γ and radiotherapy can enhance immu⁃ A/B Requires standardized EV isolation，
put immunosuppression nosuppressive GBM ⁃ EV involving PD ⁃ L1/ tumor⁃source attribution，and EV⁃PD⁃
IDO1 and macrophage PD⁃L1 modulation L1 quantification
MHC ⁃ Ⅰ anti⁃ Functional antigen ⁃ MHC⁃Ⅰ/HLA downregulation has been re⁃ B Total MHC⁃Ⅰ，membrane MHC⁃I，
gen presentation presentation visibility ported in GBM/high⁃grade glioma and may functional pMHC⁃Ⅰ，and T⁃cell rec⁃
relate to prognosis or recurrence ognition should be distinguished
MHC ⁃ Ⅰ sur⁃ Functional membrane Direct GBM evidence remains limited for C Mechanistic insight from non ⁃ GBM
face accessibili⁃ visibility glycosphingolipid shielding，SUMOylation， studies；not established as GBM⁃spe⁃
ty and PCSK9⁃related regulation cific regulation
CD47⁃SIRPα Innate immune visibi ⁃ Blocking or reducing CD47 enhances mac⁃ A Translation is limited by BBB/BBTB
axis lity rophage phagocytosis in GBM models and delivery，hematologic toxicity，het⁃
can suppress tumor growth erogeneity，and myeloid⁃cell state
CD47 stabiliza⁃ Therapy ⁃ adaptive in⁃ GBM⁃related evidence supports FAO⁃RelA A/B Dependence may vary by GBM sub⁃
tion and adapta⁃ nate immune escape acetylation⁃CD47 and hypoxia/EV⁃IGFBP2⁃ type，treatment stage，metabolic state，
tion CD47 links；EGFR/c ⁃ Src ⁃ CD47 stabiliza⁃ and hypoxic niche
tion is mechanistically relevant
GBM ⁃ EV im⁃ Distributed immune GBM⁃EV can carry PD⁃L1，IDO1，IGFBP2， A/B Tumor ⁃ derived EV must be distin⁃
mune repro⁃ suppression and moni⁃ nucleic acids，and metabolic cargo and reg⁃ guished from non ⁃ tumor EV；pro⁃
gramming toring ulate myeloid phenotypes spective clinical validation is requ ⁃
ired
PTM⁃driven EV Remote transfer of mem ⁃ Direct GBM evidence is insufficient for PTM⁃ C Mainly from general EV biology or
cargo sorting brane⁃associated signals driven EV cargo sorting non ⁃ GBM models；suitable as a fu⁃
ture research direction
A：direct GBM evidence from tissue samples，primary cells，animal models，or clinical studies；level B：high⁃grade glioma or partial GBM⁃related
evidence requiring further validation；level C：evidence mainly from pan⁃cancer，non⁃GBM，or basic cell biology studies.

Conflict of Interests： script. All authors read and approved the final manuscript.
All authors declare that they have no conflicts of interest.
［参考文献］
作者贡献声明：
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