Use of an anti-CD200-blocking antibody improves immune responses to AML in vitro and in vivo.
Namrata RastogiSarah BakerStephen T ManRobert A UgerMark WongSteven J ColesMarie HodgesAmanda F GilkesSteven KnapperRichard L DarleyAlex TonksPublished in: British journal of haematology (2020)
Treatment of relapsed/resistant acute myeloid leukaemia (AML) remains a significant area of unmet patient need, the outlook for most patients remaining extremely poor. A promising approach is to augment the anti-tumour immune response in these patients; most cancers do not activate immune effector cells because they express immunosuppressive ligands. We have previously shown that CD200 (an immunosuppressive ligand) is overexpressed in AML and confers an inferior overall survival compared to CD200low/neg patients. Here we show that a fully human anti-CD200 antibody (TTI-CD200) can block the interaction of CD200 with its receptor and restore AML immune responses in vitro and in vivo.
Keyphrases
- immune response
- end stage renal disease
- acute myeloid leukemia
- chronic kidney disease
- newly diagnosed
- ejection fraction
- dendritic cells
- prognostic factors
- bone marrow
- acute lymphoblastic leukemia
- cell proliferation
- induced apoptosis
- intensive care unit
- acute respiratory distress syndrome
- inflammatory response
- drug induced
- young adults
- regulatory t cells
- endoplasmic reticulum stress
- combination therapy
- type iii
- patient reported
- diffuse large b cell lymphoma