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La decocción modificada de Shenlingbaizhu suprime el cáncer de colon mejorando la diferenciación de las células Tfh
Gurong Jiang1, Xinyi Yan1, Yeyun Zheng1
1The Key Laboratory of Molecular Biology, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Background:
The late-stage clinical trial of immune checkpoint inhibitor (ICI) shows poor response in microsatellite stable (MSS) colorectal cancer patients. Developing effective therapeutic strategies to enhance and prolong antitumor activity remains a significant challenge for tumor types characterized by poor T-cell infiltration.
Purpose:
This study aims to explore if Modified Shenlingbaizhu Decoction (MSD) regulates anti-tumor immune response in the tumor microenvironment (TME).
Methods:
The components of MSD extracts were characterized by high performance liquid chromatography (HPLC) analysis. Single-cell RNA sequencing (scRNA-seq), flow cytometry analysis and immunofluorescence were adopted to resolve the immune landscape in MSS mice model. Enzyme-linked immunosorbent assay (ELISA) was used to detect the concentration of serum IgG.
Results:
MSD promoted antitumor immunity by increasing memory-like follicular helper T cells (Tfh) and B cells in mouse colon adenocarcinoma (COAD) tumors, rather than through CD8+ T cells or myeloid cells. Analysis of scRNA-seq results suggested MSD enhanced the secretion of CCL20 and CXCL13. Neutralizaion of CCL20 impaired the effects of MSD in promoting the migration of high endothelial venules (HEV)-associated B cells into tumor nests and facilitating the formation of tumor-associated aggregates (TAAs). Depletion of B cells reduced the generation of memory-like Tfh cells and impaired their stemness, thereby attenuated the therapeutic efficacy of MSD in COAD-bearing mice. During secondary immune responses, memory-like Tfh cells could rapidly transition to an effector state, promoting B cell differentiation into plasma cells and enhancing IgG antibody secretion. Mechanically, MSD upregulated Jarid2 expression in Tfh cells. Knockdown of Jarid2 in Tfh cells led to a decrease in the number of memory-like Tfh cells with stemness, and reduced the expression of the key receptor ICOS that interacted with B cells.
Conclusions:
Mutual interaction between B cells and memory-like Tfh cells was promising immune response for the treatment of MSS COAD. MSD promoted the formation of TAA to intensify Tfh cell/B cell collaboration in a CCL20 dependent-manner.
