<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xu H</submitter><funding>Shandong Provincial Natural Science Foundation</funding><funding>Chinese Society of Clinical Oncology-Gilead Cancer Research Foundation</funding><funding>Wu Jieping Medical Foundation</funding><funding>Natural Science Foundation of Shandong Province</funding><funding>National Natural Science Foundation of China</funding><funding>Beijing Science and Technology Innovation Medical Development Foun-dation</funding><funding>Key R&amp;D Program of Shandong Province</funding><funding>the Jinan Science and Technology Innovation Program of Clinical Medicine</funding><funding>Health Commission of Anhui Province Scientific Research Project</funding><pagination>2225-2236</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11970544</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>156(11)</volume><pubmed_abstract>Immune checkpoint inhibitors (ICIs) have shifted the treatment paradigm of non-small cell lung cancer (NSCLC) over the last decade. Despite notable therapeutic advancements in responders, the response rate remains limited owing to the immunosuppressive tumor microenvironment (TME). Therefore, to improve the efficacy of ICIs, it is essential to explore alternative targets or signals that mediate immunosuppression. Immunoglobulin-like transcript (ILT) 5 is a negative regulator of immune activation in myeloid cells. However, the expression and function of ILT5 in NSCLC remain unknown. Here, we found that ILT5 was highly expressed in tumor-associated macrophages (TAMs) of NSCLC tissues and predicted poor patient survival. Functionally, ILT5 induces the M2-like polarization of TAMs, which subse</pubmed_abstract><journal>International journal of cancer</journal><pubmed_title>Immunoglobulin-like transcript 5 polarizes M2-like tumor-associated macrophages for immunosuppression in non-small cell lung cancer.</pubmed_title><pmcid>PMC11970544</pmcid><funding_grant_id>2022CXGC010510</funding_grant_id><funding_grant_id>ZR2021MH268</funding_grant_id><funding_grant_id>82103340</funding_grant_id><funding_grant_id>82103466</funding_grant_id><funding_grant_id>320.6750.2023-05-51</funding_grant_id><funding_grant_id>202225015</funding_grant_id><funding_grant_id>320.6750.2023‐05‐51</funding_grant_id><funding_grant_id>AHWJ2023BAc10031</funding_grant_id><funding_grant_id>202134041</funding_grant_id><funding_grant_id>AHWJ2023A30183</funding_grant_id><funding_grant_id>KC2023-JX-0288-PQ88</funding_grant_id><funding_grant_id>Y-Gilead2024-PT-0148</funding_grant_id><pubmed_authors>Gao A</pubmed_authors><pubmed_authors>Zhang F</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>He Y</pubmed_authors><pubmed_authors>Fu X</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Ge Y</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Xu H</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immunoglobulin-like transcript 5 polarizes M2-like tumor-associated macrophages for immunosuppression in non-small cell lung cancer.</name><description>Immune checkpoint inhibitors (ICIs) have shifted the treatment paradigm of non-small cell lung cancer (NSCLC) over the last decade. Despite notable therapeutic advancements in responders, the response rate remains limited owing to the immunosuppressive tumor microenvironment (TME). Therefore, to improve the efficacy of ICIs, it is essential to explore alternative targets or signals that mediate immunosuppression. Immunoglobulin-like transcript (ILT) 5 is a negative regulator of immune activation in myeloid cells. However, the expression and function of ILT5 in NSCLC remain unknown. Here, we found that ILT5 was highly expressed in tumor-associated macrophages (TAMs) of NSCLC tissues and predicted poor patient survival. Functionally, ILT5 induces the M2-like polarization of TAMs, which subse</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jun</publication><modification>2026-07-15T11:02:15.053Z</modification><creation>2025-07-09T03:05:05.651Z</creation></dates><accession>S-EPMC11970544</accession><cross_references><pubmed>39910654</pubmed><doi>10.1002/ijc.35360</doi></cross_references></HashMap>