TY - JOUR T1 - Immune-Checkpoint expression on CD4, CD8 and NK cells in blood, BAL and lymph nodes of sarcoidosis JF - ERJ Open Research JO - erjor DO - 10.1183/23120541.LSC-2022.155 VL - 8 IS - suppl 8 SP - 155 AU - Miriana D'Alessandro AU - Laura Bergantini AU - Fabrizio Mezzasalma AU - Edoardo Conticini AU - Dalila Cavallaro AU - Sara Gangi AU - Stefano Cattelan AU - Elena Bargagli AU - Paolo Cameli Y1 - 2022/03/10 UR - http://openres.ersjournals.com/content/8/suppl_8/155.abstract N2 - Introduction: Sarcoidosis is a granulomatous disorder of unknown origin characterized by non-necrotizing granulomas with activated CD4 cell. T cell activation is regulated by co-stimulatory and co-inhibitory factors: immune-checkpoint (IC) molecules.Aim and Objectives: Here we compared expression of IC molecules on CD4, CD8 and NK cells from peripheral blood (PBMC), bronchoalveolar lavage (BAL) and lung‐draining lymph node (LLN) samples of sarcoidosis patients (SP) as well as their expression in PBMC from SP and healthy controls (HC).Methods: Flowcytometry analysis was performed to detect IC molecules and machine learning approach for statistic.Results: Higher CD4 percentages were observed in LLN than in PBMC, while CD8 percentages were lower in LLN than in PBMC and BAL. Higher PD1 expression on CD4 was observed in BAL than in LLN as well as on CD8 from BAL than from LLN and PBMC. CTLA4expression on CD4 was higher in LLN than in BAL as well as on CD8. TIGIT expression on CD4 were more abundant in BAL than in PBMC, while it was expressed on CD8 in PBMC than in BAL. NK were higher in PBMC than in LLN and BAL. Higher fraction of CD56TIGIT in LLN than in PBMC. The best clustering variables through a decision-tree model was: CD4PD1followed by CD4TIGIT, CD3, CD8CTLA4. When the peripheral cell subsets of SP and HC were used, the best clustering variables were CD56TIGITConclusion: Although the detailed mechanism of the present findings remains unclear, high expression of PD1 and TIGIT on T cells in BAL, as well as CTLA4 and TIGIT on T cells in LLN, suggest that inhibition of these molecules could be a therapeutic strategy for avoiding the development of chronic inflammation and tissue damage in SPFootnotesCite this article as ERJ Open Research 2022; 8: Suppl. 8, 155.This article was presented at the 2022 ERS Lung Science Conference, in session “Poster Session 2”.This is an ERS Lung Science Conference 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). ER -