| 背景 | Anti-Human TIGIT (clone IB16) is a fully human IgG1 monoclonal antibody directed against human TIGIT (T-cell immunoreceptor with Ig and ITIM domains), an inhibitory checkpoint receptor. The human IgG1 framework makes this clone well suited to studies that require an intact human Fc, including engagement of human Fc-gamma receptors and complement, ADCC/ADCP readouts, and mechanistic work on how anti-TIGIT antibodies modulate T-cell and NK-cell activity in human systems. Because the antibody recognises human TIGIT, it is appropriate for in-vitro functional assays on primary human lymphocytes, humanised or engineered cell lines, and human tumour-immune co-culture models, as well as for binding, blocking, and flow-cytometry applications. It is supplied low-endotoxin, bulk (mg to gram scale), and research-use-only, so it is a practical choice for functional and larger-scale experiments where lot-to-lot consistency and low endotoxin matter. Species reactivity is human; investigators working in mouse models should confirm cross-reactivity and select a suitable surrogate clone where needed.
TIGIT is a co-inhibitory receptor of the immunoglobulin superfamily expressed on activated and memory T cells, regulatory T cells, follicular helper T cells, and natural killer cells. It contains an extracellular IgV domain and a cytoplasmic tail bearing ITIM and ITT-like motifs that transmit inhibitory signals. TIGIT binds the nectin-family ligands CD155 (PVR) and, with lower affinity, CD112 (PVRL2/nectin-2), which are frequently upregulated on tumour cells and antigen-presenting cells. TIGIT competes with the co-stimulatory receptor CD226 (DNAM-1) for these shared ligands; because TIGIT binds CD155 with higher affinity, it can outcompete CD226 and shift the balance toward immune suppression. Engagement dampens T-cell and NK-cell effector function, promotes regulatory T-cell activity, and contributes to T-cell exhaustion. TIGIT is a prominent target in cancer immunotherapy and is often co-expressed with PD-1, motivating combination-blockade strategies. |
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