Viewing negative mentions of gene expression of ICAM1 (H. sapiens) in T cells

Full-text article links are indicated by after the article reference.

Document Target Regulator Anatomy Sentence
Liu et al. (2009)ICAMT-cellMoreover, pancreatic cancer cells expressing neither ICAM-1 nor ICAM-2 were bound poorly by gammadelta-T cells and were found to be resistant to gammadelta-T-cell killing.
Batten et al. (1995)ICAM-1T cellsDAP.3 transfectants expressing native H-2E molecules with or without human LFA-3 and ICAM-1 (intercellular adhesion molecule-1) failed to induce proliferation by human peripheral blood T cells.
Perez et al. (2007)ICAMT cell1 was decreased when cells were treated with CD3/CD28 plus ICAM-2 or ICAM-3, but not ICAM-1, indicating that different ICAMs can alter cytokine production that can influence TH1/TH2 T cell development.
Tohma et al. (1992)ICAM-1T cellsResting CD4+ T cells were largely ICAM-1 negative, whereas immobilized anti-CD3 monoclonal antibody (mAb) rapidly induced ICAM-1 expression.
Trejdosiewicz (1992)ICAM-1IELAs normal and inflamed intestinal epithelia do not express ICAM-1, it seems unlikely that the LFA-1/ICAM-1 interaction is of importance to IEL activation.
Damle et al. (1993)intercellular adhesion molecule-1T cellsAlloAg-primed CD4+ T cells, which expressed both class II MHC and intercellular adhesion molecule-1 but not B7, presented SAg to and induced proliferation of both resting and SAg-primed T cells.
Gerli et al. (1993)ICAM-1T cellsDespite the fact that ICAM-1 and LFA-3 molecules were virtually absent on cord resting T cells, mAb against these two molecules boosted both mitogenesis of and interleukin (IL)-2 production by purified cord T cells stimulated with plastic immobilized anti-CD3.
Kerkhoff et al. (1993)CD54T cellsT cells were negative for CD25, CD54 and major histocompatibility complex (MHC)-class II.