<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jiang F</submitter><funding>National Natural Science Foundation of China</funding><funding>Beijing Natural Science Foundation</funding><pagination>4311</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9455014</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(17)</volume><pubmed_abstract>Endometrial carcinoma (EC) is a gynecological malignancy with a high incidence; however, thorough studies on tumor-infiltrating lymphocyte (TIL) populations in EC are lacking. We aimed to map the immune atlas of TILs in type I EC via single-cell RNA sequencing (scRNA-seq), mass cytometry and flow cytometry analysis. We found that natural killer (NK) cells and CD8+ T lymphocytes were the major components of TILs in EC patients. We first identified three transcriptionally distinct NK cell subsets, which are likely to possess diverse anti-tumor functions. Additionally, CD103+ cells substantially contributed to the CD8+ T cell population. The signature gene expression of CD103+ CD8+ T cells indicated the tissue residency, immunological memory, and exhaustion properties of this cell subset, which were defined as tissue-resident memory T cells (T&lt;sub>RM&lt;/sub> cells). Moreover, based on scRNA-seq and mass cytometry analysis, we first identified the intrinsic heterogeneity of CD103+ CD8+ T cells that were thought to have a distinct cytotoxicity, cell adhesion and exhaustion status functions. Collectively, distinct subsets of NK cells were found and might shed light on future investigations. CD103+ CD8+ T cell population may be an important immunotherapeutic target in EC and targeting this cell population with combined immunosuppressive therapy might improve the efficacy of immunotherapy for EC.</pubmed_abstract><journal>Cancers</journal><pubmed_title>Single-Cell Profiling of the Immune Atlas of Tumor-Infiltrating Lymphocytes in Endometrial Carcinoma.</pubmed_title><pmcid>PMC9455014</pmcid><funding_grant_id>82071760</funding_grant_id><funding_grant_id>7222126</funding_grant_id><pubmed_authors>Mao M</pubmed_authors><pubmed_authors>Yu M</pubmed_authors><pubmed_authors>Jiang F</pubmed_authors><pubmed_authors>Yang K</pubmed_authors><pubmed_authors>Cao D</pubmed_authors><pubmed_authors>Xiang Y</pubmed_authors><pubmed_authors>Jiao Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Single-Cell Profiling of the Immune Atlas of Tumor-Infiltrating Lymphocytes in Endometrial Carcinoma.</name><description>Endometrial carcinoma (EC) is a gynecological malignancy with a high incidence; however, thorough studies on tumor-infiltrating lymphocyte (TIL) populations in EC are lacking. We aimed to map the immune atlas of TILs in type I EC via single-cell RNA sequencing (scRNA-seq), mass cytometry and flow cytometry analysis. We found that natural killer (NK) cells and CD8+ T lymphocytes were the major components of TILs in EC patients. We first identified three transcriptionally distinct NK cell subsets, which are likely to possess diverse anti-tumor functions. Additionally, CD103+ cells substantially contributed to the CD8+ T cell population. The signature gene expression of CD103+ CD8+ T cells indicated the tissue residency, immunological memory, and exhaustion properties of this cell subset, which were defined as tissue-resident memory T cells (T&lt;sub>RM&lt;/sub> cells). Moreover, based on scRNA-seq and mass cytometry analysis, we first identified the intrinsic heterogeneity of CD103+ CD8+ T cells that were thought to have a distinct cytotoxicity, cell adhesion and exhaustion status functions. Collectively, distinct subsets of NK cells were found and might shed light on future investigations. CD103+ CD8+ T cell population may be an important immunotherapeutic target in EC and targeting this cell population with combined immunosuppressive therapy might improve the efficacy of immunotherapy for EC.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2025-07-25T03:07:57.852Z</modification><creation>2025-07-25T03:07:57.852Z</creation></dates><accession>S-EPMC9455014</accession><cross_references><pubmed>36077846</pubmed><doi>10.3390/cancers14174311</doi></cross_references></HashMap>