CD200 Inhibits Memory Th1 Cell Function in Acute Myeloid Leukaemia (AML)

Coles, Steven ORCID: https://orcid.org/0000-0002-1109-6971, Man, S., Hills, R.K., Wang, E.C.Y., Burnett, A.K., Darley, R.L. and Tonks, A. (2011) CD200 Inhibits Memory Th1 Cell Function in Acute Myeloid Leukaemia (AML). In: Annual Congress of the British Society for Immunology, 5th - 8th December 2011, Liverpool, UK. (Unpublished)

Abstract

CD200 is a cell-surface glycoprotein that is normally expressed in tissues of the immune system, where its role is to protect immune privileged sites. We previously established CD200 to be frequently over-expressed and associated with poor AML patient outcome. In
this study, we investigated the possibility that CD200 expression may mediate suppression of T-cell function in this disease. Using multiparameter flow cytometry, we compared PMA/ionomycin stimulated CD8+ T-cell cytotoxic potential (CD107a expression) and the frequency
of intracellular TNFa, IL-2 and IFNc producing CD4+/CD8+
memory T-cells between CD200hi and CD200lo patients. We demonstrated that both the magnitude of the CD8+ memory cytotoxic T-cell response and the Th1 cytokine producing CD4+ memory helper T-cells was significantly inhibited in CD200hi AML patients (P < 0.05). Further, using ELISPOT assays to measure IFNg release we showed that the Th1 memory response to common viral antigens was significantly reduced by 75% in CD200hi versus CD200lo AML patients(P < 0.05). Recovery of IFNc release in response to recall antigens
was observed in CD4+ memory T-cells incubated with a
blocking antibody to CD200R. In conclusion, this study shows a correlation between T-cell dysfunction and expression of CD200 which suggests targeting this axis could be therapeutically beneficial for AML CD200hi patients.

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