Supplementary Table S1 from Tertiary Lymphoid Structures Are Associated with Enhanced Macrophage Activation and Immune Checkpoint Expression and Predict Outcome in Cervical Cancer
posted on 2025-05-02, 07:22authored byLaurent Gorvel, Marylou Panouillot, Marie-Sarah Rouvière, Emilien Billon, Stéphane Fattori, Jumaporn Sonongbua, Nicolas Boucherit, Amira Ben Amara, Olivia Quilichini, Samuel Granjeaud, Clara Degos, Jacques A. Nunès, Xavier Carcopino, Eric Lambaudie, Anne-Sophie Chrétien, Renaud Sabatier, Marie-Caroline Dieu-Nosjean, Daniel Olive
Samples used in each experiment
Funding
Fondation de France (Foundation of France)
Fondation ARC pour la Recherche sur le Cancer (ARC)
Assistance Publique - Hopitaux de Marseille
History
ARTICLE ABSTRACT
Cervical tumors are usually treated using surgery, chemotherapy, and radiotherapy and would benefit from immunotherapies. However, the immune microenvironment in cervical cancer remains poorly described. Tertiary lymphoid structures (TLS) were recently described as markers for better immunotherapy response and overall better prognosis in patients with cancer. We evaluated the cervical tumor immune microenvironment, specifically focusing on TLS, using combined high-throughput phenotyping, soluble factor concentration dosage in the tumor microenvironment, and spatial interaction analyses. We found that TLS presence was associated with a more inflammatory soluble microenvironment, with the presence of B cells as well as more activated macrophages and dendritic cells (DC). Furthermore, this myeloid cell activation was associated with the expression of immune checkpoints, such as PD-L1 and CD40, and the proximity of activated conventional type 2 DCs to CD8+ T cells, indicating better immune interactions and tumor control. Finally, we associated TLS presence, greater B-cell density, and activated DC density with improved progression-free survival, substantiating TLS presence as a potential prognostic marker. Our results provide evidence that TLS presence denotes cell activation and immunotherapy target expression.