Anti-CD3 Antibody (UCHT-1)

Anti-CD3 Antibody (UCHT-1) (10 μg/mL) significantly elevates the intracellular free calcium concentration in freshly isolated human primary T lymphocytes from a basal level of 32.5 nM to 112 nM^[1].
Anti-CD3 Antibody (UCHT-1) (10 μg/mL; 10 min) activates phosphoinositide 3-kinase in purified human primary T lymphocytes^[1].
Anti-CD3 Antibody (UCHT-1) (1 μL of 1-mg/mL solution per million WBCs; ~30 min) eliminates human T cells while preserving non-T human cell populations in unfractionated human UCB WBCs^[2].
Anti-CD3 Antibody (UCHT-1) (0.01-1 μg/mL; 3-24 h incubation, 1-3 days culture) induces time- and dose-dependent modulation of T3 antigenic sites on PBMC from UCHT1-nonresponsive human donors, with complete depletion at 1 μg/mL after 6 h, and T3-reexpressing cells regain partial proliferative responsiveness to PHA in parallel with T3 reexpression^[3].
Anti-CD3 Antibody (UCHT-1) (1-10000 ng/mL; 1-6 days) triggers mitogenic proliferation in PBMC from 62.5% of healthy adult donors (80% male, 45% female) via an IL 2-independent mechanism, with optimal activity at 100 ng/mL over 3 days^[4].
Anti-CD3 Antibody (UCHT-1) (100 ng/mL; 3 days)-induced proliferation in PBMC from responsive healthy donors at 100 ng/mL over 3 days is not inhibited by anti-Tac antibody, confirming an IL₂-independent mechanism^[4].
Anti-CD3 Antibody (UCHT-1) (1 μg/mL) induces a biphasic [Ca²⁺]_i response in human peripheral blood T lymphocytes, with an initial transient peak from intracellular Ca²⁺ release and a sustained plateau from extracellular Ca²⁺ influx; the transient peak is eliminated by intracellular BAPTA buffering^[5].
Anti-CD3 Antibody (UCHT-1) (0.01-10 μg/mL; 10 min pre-incubation, 3-6 days culture) potently suppresses proliferation of PBMC and T cells from UCHT1-nonresponsive human donors induced by PHA, Concanavalin A (Con A) (HY-P2149), Candidin (HY-182559), or allogeneic non-T cells^[3].
Anti-CD3 Antibody (UCHT-1) (1 μg/mL; added at culture initiation or 0-48 h post-stimulation, 3-6 days culture) maximally abrogates proliferation of PHA-stimulated PBMC and allogeneic non-T cell-stimulated T cells from UCHT1-nonresponsive human donors only when added at culture initiation, with no inhibitory effect when added 24 h (PHA) or 48 h (allogeneic non-T cells) post-stimulation^[3].
Anti-CD3 Antibody (UCHT-1) (1 μg/mL) almost completely abrogates IL-2 production by PBMC stimulated with PHA and T cells stimulated with allogeneic non-T cells from UCHT1-nonresponsive human donors across all tested time points^[3].
Anti-CD3 Antibody (UCHT-1) (1 μg/mL; continuous incubation, 1-3 days culture) completely blocks IL-2 receptor expression on PHA-stimulated PBMC from UCHT1-nonresponsive human donors over 3 days of culture^[3].
Anti-CD3 Antibody (UCHT-1) (100 ng/mL; 1-3 days) induces IL₂ receptor expression in 65-72% of PBMC from responsive healthy donors after 2-3 days of incubation at 100 ng/mL, but fails to induce meaningful IL₂ receptor expression in PBMC from non-responsive donors^[4].
Anti-CD3 Antibody (UCHT-1) (1 μg/mL; 15 min, 1 h) induces full IL-2 secretion, IL-2 receptor expression, and proliferation in human peripheral blood mononuclear cells with extracellular Ca²⁺, even when intracellular Ca²⁺ release-mediated transient [Ca²⁺]_i peaks are buffered by BAPTA; extracellular Ca²⁺ is required for IL-2 secretion and proliferation but not IL-2 receptor expression^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.