| 背景 | Anti-Human TIM-3 (IB19) is a recombinant human IgG4 (S228P) kappa antibody directed against human TIM-3 (HAVCR2, UniProt Q8TDQ0). The human IgG4 framework with the stabilizing S228P hinge mutation reduces Fab-arm exchange and minimizes effector function, making the format well suited to receptor-blockade and checkpoint-modulation studies where cross-linking or Fc-mediated depletion is undesirable. Supplied as a low-endotoxin, bulk (mg to g) research-grade preparation, it is intended for research use only and is appropriate for functional and mechanistic in-vitro work with human cells, ex-vivo studies of primary human lymphocytes and tumour-infiltrating populations, and comparative/benchmarking work against clinical-stage anti-TIM-3 agents. Its human-only reactivity and therapeutic-style format make it a practical reagent for immuno-oncology and immune-exhaustion research, flow cytometry, binding and blocking assays, and screening pipelines. Because it targets human TIM-3, standard mouse in-vivo dosing regimens are not directly applicable; investigators using humanized or human-cell models should establish their own conditions empirically.
TIM-3 (T-cell immunoglobulin and mucin-domain containing-3; HAVCR2, UniProt Q8TDQ0) is a type I transmembrane receptor of the TIM family, expressed on exhausted and terminally differentiated CD8+ and CD4+ T cells, Tregs, NK cells, and myeloid populations including dendritic cells. It functions as a co-inhibitory checkpoint that dampens effector responses upon engagement of ligands such as galectin-9, phosphatidylserine, HMGB1, and CEACAM1. TIM-3 lacks classical inhibitory motifs; signaling is instead regulated through its cytoplasmic tail and interactions with adaptors such as Bat3, whose release upon ligand binding promotes an exhausted phenotype. TIM-3 is frequently co-expressed with PD-1 on dysfunctional tumour-infiltrating lymphocytes, marking a deeply exhausted state, and is an actively pursued immuno-oncology target. It also contributes to innate immune regulation and tolerance, and dysregulation is implicated in cancer, chronic viral infection, and autoimmunity. |
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