mononuclear cell

Myelin Basic Protein (87-99) Acetate (Myelin Basic Protein (87-99) Acetate (118506-26-6 Free base)) is an encephalitogenic peptide that induces basic protein-specific T cell proliferation. Myelin Basic Protein (87-99) Acetate causes a Th1 polarization in peripheral blood mononuclear cells, which is implicated in multiple sclerosis (MS).

HOXB7 (8-25), a peptide fragment derived from homeobox B7 (HOXB7)—a key controller of cell growth and oncogene activator—facilitates antigen presentation when pulsed onto dendritic cells obtained from human peripheral blood mononuclear cells (PBMCs). This process promotes the activation and interferon-gamma (IFN-γ) production by CD4+ helper T cells, triggering targeted and broad-spectrum antitumor responses.

Myelin Basic Protein (87-99) TFA, an encephalitogenic peptide, promotes basic protein-specific T cell proliferation and induces Th1 polarization in peripheral blood mononuclear cells, contributing to the pathogenesis of multiple sclerosis (MS) [1] [2].

EGFRvIII peptide, a synthetic peptide mirroring the EGFRvIII fusion junction—a tumor-specific, perpetually active EGFR variant missing amino acids 6-273 of the wild-type—binds to HLA-A*0201-positive T2 cells under MHC class I at 25 µg/ml. It enables antigen presentation in dendritic cells from human peripheral blood mononuclear cells (PBMCs), thus activating CD8+ cytotoxic T lymphocytes and prompting IFN-γ production. Administered at 15 µg/animal with the TLR5 agonist flagellin B, EGFRvIII peptide elevates CD8+ T cell numbers, lowers regulatory T cells (Tregs) in the brain, diminishes tumor volume, and extends survival in a GL261 glioblastoma mouse model.

SDF-1α (human) serves as a chemotactic agent for mononuclear cells through its interaction with the CXCR4 receptor, facilitating critical biological processes such as stem cell homing, retention, survival, and proliferation, in addition to cardiomyocyte repair, angiogenesis, and ventricular remodeling post-myocardial infarction. It holds significant utility in cardiovascular disease research [1] [2].

Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78) serves as a T cell proliferation activator by promoting the dose-dependent in vitro proliferation of human peripheral blood mononuclear cells (PBMC) and is used in research on inflammation, immunity, and cancer [1].

BMSpep-57, a potent macrocyclic peptide inhibitor, competitively disrupts the PD-1 PD-L1 interaction, demonstrating a significant inhibitory concentration (IC50) of 7.68 nM. It exhibits binding affinity towards PD-L1 with dissociation constants (Kd) of 19 nM and 19.88 nM in MicroScale Thermophoresis (MST) and Surface Plasmon Resonance (SPR) assays, respectively. This compound enhances T cell functionality by promoting Interleukin-2 (IL-2) production within Peripheral Blood Mononuclear Cells (PBMCs).