Replies to post #221 on Fate Therapeutics Inc (FATE)

[jondoeuk]

Naturally, HLA-G blocks immune cell function by binding the inhibitory receptors ILT2 and ILT4. All active isoforms of HLA-G must engage the D1 and D2 domains of ILT2 and ILT4. So, to overcome this, extracellular domains from ILT2 or ILT4 that bind with HLA-G are fused with intracellular signaling domains that activate NK cell function. NKILT's activation mechanism utilises the disulphide-linked dimerisation of HLA-G to promote CIR dimerisation and NK cell activation.

[jondoeuk]

The SITC presentation highlighted the latest updates on NKILT Therapeutics' engineered CIR-NK cells with proof-of-concept in vitro data against leukaemia cells expressing HLA-G https://jitc.bmj.com/content/11/Suppl_1/A290

The ASH, an oral presentation will feature details of the proprietary activation domains that enhance activity of the CIR-NK engineered cells against HLA-G-positive acute myeloid leukaemia cells. The presentation will expand preclinical data with a specific focus on these novel activation domains and will characterise the serial killing activity against AML cells https://ash.confex.com/ash/2023/webprogram/Paper190073.html