<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Aggarwal R</submitter><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIAMS NIH HHS</funding><pagination>2133-44</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3939063</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>133(9)</volume><pubmed_abstract>Innate immune system has been known to play an important role in inhibiting the malignant transformation, tumor progression and invasion. However, the mechanistic basis remains ambiguous. Despite polyclonality of human γδ T cells, Vγ2Vδ2 T cell subset was shown to recognize and limit the growth of various tumors at various degrees. The differential recognition of the tumor cells by Vγ2Vδ2 T cells are yet to be defined. Our study reveals that γδ T cells limit in vitro growth of most breast tumor cells, such as SkBr7 (HER2+), MCF7 (ER+) and MDA-MB-231 (ER-) by inhibiting their survival and inducing apoptosis, except BrCa-MZ01 (PR+) cells. To investigate detail mechanisms of antineoplastic effects, we found that cell death was associated with the surface expression levels of MICA/B and ICAM1.</pubmed_abstract><journal>International journal of cancer</journal><pubmed_title>Human Vγ2Vδ2 T cells limit breast cancer growth by modulating cell survival-, apoptosis-related molecules and microenvironment in tumors.</pubmed_title><pmcid>PMC3939063</pmcid><funding_grant_id>P30 CA016058</funding_grant_id><funding_grant_id>K12 CA133250</funding_grant_id><funding_grant_id>R44 HL092706</funding_grant_id><funding_grant_id>R44 HL092706-01</funding_grant_id><funding_grant_id>R21 CA143787</funding_grant_id><funding_grant_id>K01 AR054114</funding_grant_id><pubmed_authors>Das H</pubmed_authors><pubmed_authors>Kanji S</pubmed_authors><pubmed_authors>Aggarwal R</pubmed_authors><pubmed_authors>Lu J</pubmed_authors><pubmed_authors>Joseph M</pubmed_authors><pubmed_authors>Pompili VJ</pubmed_authors><pubmed_authors>Shapiro CL</pubmed_authors><pubmed_authors>Ray A</pubmed_authors><pubmed_authors>Lustberg MB</pubmed_authors><pubmed_authors>Das M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Human Vγ2Vδ2 T cells limit breast cancer growth by modulating cell survival-, apoptosis-related molecules and microenvironment in tumors.</name><description>Innate immune system has been known to play an important role in inhibiting the malignant transformation, tumor progression and invasion. However, the mechanistic basis remains ambiguous. Despite polyclonality of human γδ T cells, Vγ2Vδ2 T cell subset was shown to recognize and limit the growth of various tumors at various degrees. The differential recognition of the tumor cells by Vγ2Vδ2 T cells are yet to be defined. Our study reveals that γδ T cells limit in vitro growth of most breast tumor cells, such as SkBr7 (HER2+), MCF7 (ER+) and MDA-MB-231 (ER-) by inhibiting their survival and inducing apoptosis, except BrCa-MZ01 (PR+) cells. To investigate detail mechanisms of antineoplastic effects, we found that cell death was associated with the surface expression levels of MICA/B and ICAM1.</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Nov</publication><modification>2025-07-10T03:08:35.111Z</modification><creation>2025-07-10T03:08:35.111Z</creation></dates><accession>S-EPMC3939063</accession><cross_references><pubmed>23595559</pubmed><doi>10.1002/ijc.28217</doi></cross_references></HashMap>