NK cell activation & innate cytotoxicity
NK cell activation & innate cytotoxicity. A natural killer cell integrates opposing signals at the immune synapse: activating receptors (NKG2D, CD16, NKp46, DNAM-1) read stress ligands and antibody-coated targets, while inhibitory receptors (KIR, NKG2A) sense self MHC-I. When activating input outweighs inhibition — the “missing-self” rule — the NK cell releases perforin and granzyme B and secretes IFN-γ. Click any protein for the matching Assay Genie In Vivo functional-grade antibody or ELISA kit.
NK cells do not need prior sensitisation. Instead they weigh activating against inhibitory signals in real time. NKG2D recognises stress-induced ligands (MICA/B, ULBP); CD16 (FcγRIII) binds antibody-coated targets to trigger ADCC; NKp46 is a natural cytotoxicity receptor; and DNAM-1 engages CD155/CD112. Their ITAM adaptors (DAP12/CD3ζ, with DAP10 for NKG2D) recruit SYK and PI3K to build the activation signal.
Healthy cells display self MHC-I, which engages KIR and NKG2A. Their ITIMs recruit the phosphatase SHP-1, which dephosphorylates the activating machinery and vetoes the response — self-tolerance. Virally infected or transformed cells that lose MHC-I or up-regulate stress ligands tip the balance toward activation (the “missing-self” principle).
Once activation wins, the NK cell releases cytotoxic granules — perforin pores let granzyme B enter and trigger target-cell apoptosis — and secretes IFN-γ and TNF-α to shape the wider immune response. Assay Genie In Vivo functional-grade anti-IFN-γ and anti-TNF-α neutralise those cytokines, with ELISA kits and antibodies covering every receptor, adaptor and effector. For research use only; not for diagnostic or therapeutic procedures. Mouse targets shown where available.
Every protein node links to a product: In Vivo anti-IFN-γ / anti-TNF-α for the cytokine outputs; receptors, adaptors, kinases and cytolytic effectors open the matching ELISA kit or antibody.