RT Journal Article
SR Electronic
T1 Dendritic cells are defective for improving survival in lung adenocarcinoma
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP OA778
DO 10.1183/13993003.congress-2023.OA778
VO 62
IS suppl 67
A1 Zimermam, Heloisa
A1 Setembre Batah, Sabrina
A1 Faci Do Marco, Maria Júlia
A1 Magalhães Lage Moraes, Mateus
A1 Tadao Wada, Danilo
A1 Brito Silva, Saulo
A1 Todorovic Fabro, Alexandre
YR 2023
UL http://erj.ersjournals.com/content/62/suppl_67/OA778.abstract
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).