PT  - JOURNAL ARTICLE
AU  - Zimermam, Heloisa
AU  - Setembre Batah, Sabrina
AU  - Faci Do Marco, Maria Júlia
AU  - Magalhães Lage Moraes, Mateus
AU  - Tadao Wada, Danilo
AU  - Brito Silva, Saulo
AU  - Todorovic Fabro, Alexandre
TI  - Dendritic cells are defective for improving survival in lung adenocarcinoma
AID  - 10.1183/13993003.congress-2023.OA778
DP  - 2023 Sep 09
TA  - European Respiratory Journal
PG  - OA778
VI  - 62
IP  - suppl 67
4099  - http://erj.ersjournals.com/content/62/suppl_67/OA778.short
4100  - http://erj.ersjournals.com/content/62/suppl_67/OA778.full
SO  - Eur Respir J2023 Sep 09; 62
AB  - Introduction: Adenocarcinoma(ADENO) and squamous cell carcinoma(SCC) are complex diseases that involves molecular alterations and immune system, which is a key regulator for immunotherapy. Dendritic cells(DC) play a critical role in the tumor microenvironment in pro-active anti-tumor immune stimulation or in a “protective” system.Aims and Objectives: To determine the dendritic cell profile in adenocarcinoma and squamous cell carcinoma.Methods: A retrospective study was carried out with 46 NSCLC lobectomy samples. A detailed evaluation of H&E slides and immunohistochemical panel for CD1a, Langerin and Mannose were performed with morphometrical analysis.Results: Survival analysis revealed that CD1a+DC has worst survival in ADENO with necrosis area less than 50%(P<0.05). Therefore, the immune stimulation of CD1a+DC and Langerin+DC in ADENO appeared as ineffective in tumor and front area. However, these immunophenotypes in SCC did not present significant participation, not affecting survival. Furthermore, both ADENO and SCC revealed Mannose+DC as an important role in the front area.Conclusions: The expression of dendritic cells in the tumor microenvironment differs between ADENO and CEC. In ADENO, some molecular mechanisms may be preventing the proper functioning of DC with immunophenotype CD1a+ and Langerin+, while in SCC, other molecular pathways may be blocking their expression.(FAPESP Nº22/02821-0, 21/09024-6, 21/10981-5, 19/01517-3).FootnotesCite this article as: European Respiratory Journal 2023; 62: Suppl. 67, OA778.This abstract was presented at the 2023 ERS International Congress, in session “Inflammatory endotyping: the macrophage across disease areas”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).