Abstract:
:CD134 (OX40) is a member of the tumour necrosis factor receptor superfamily (TNFRSF). It acts as a costimulatory receptor on T cells, but its role on NK cells is poorly understood. CD137, another TNFRSF member has been shown to enhance the anti-tumour activity of NK cells in various malignancies. Here, we examine the expression and function of CD134 on human and mouse NK cells in B-cell lymphoma. CD134 was transiently upregulated upon activation of NK cells in both species. In contrast to CD137, induction of CD134 on human NK cells was dependent on close proximity to, or cell-to-cell contact with, monocytes or T cells. Stimulation with an agonistic anti-CD134 mAb but not CD134 ligand, increased IFNγ production and cytotoxicity of human NK cells, but this was dependent on simultaneous antibody:Fcγ receptor binding. In complementary murine studies, intravenous inoculation with BCL1 lymphoma into immunocompetent syngeneic mice resulted in transient upregulation of CD134 on NK cells. Combination treatment with anti-CD20 and anti-CD134 mAb produced a synergistic effect with durable remissions. This therapeutic benefit was abrogated by NK cell depletion and in Fcγ chain -/- mice. Hence, anti-CD134 agonists may enhance NK-mediated anti-tumour activity in an Fcγ receptor dependent fashion.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Turaj AH,Cox KL,Penfold CA,French RR,Mockridge CI,Willoughby JE,Tutt AL,Griffiths J,Johnson PWM,Glennie MJ,Levy R,Cragg MS,Lim SHdoi
10.1038/s41598-018-20656-ysubject
Has Abstractpub_date
2018-02-02 00:00:00pages
2278issue
1issn
2045-2322pii
10.1038/s41598-018-20656-yjournal_volume
8pub_type
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