BY55/CD160 cannot be considered a cytotoxic marker in cytomegalovirus- specific human CD8+ T cells

11Citations
Citations of this article
15Readers
Mendeley users who have this article in their library.
Get full text

Abstract

CD160/BY55 is a glucosyl-phosphatidylinositol (GPI)-anchored cell membrane receptor that is expressed primarily in natural killer (NK) cells. Its presence in CD8+ T lymphocytes is considered to be a marker of cytotoxic activity, although there are few data in this regard. In the present work, we analysed the expression of CD160 in subpopulations of cytomegalovirus (CMV)-specific CD8+ T cells. Subpopulations were defined by CD28 and CD57 expression and exhibited varying degrees of differentiation and cytotoxic potential, as evaluated by the expression of perforin, interferon (IFN)-γ and interleukin (IL)-7Rα/CD127. We included subjects with different intensities of anti-viral immune response. Results showed that the terminally differentiated CD28- CD57+ subset displaying the highest level of perforin expressed CD160 at a level similar to that of memory CD28 + CD57-perforin- cells. A comparison of the expression of perforin in CD160+ cells versus CD160- cells showed that expression was significantly higher in the absence of CD160. Interestingly, the CMV-specific CD8+ T cell subset from a patient with ongoing CMV reactivation did not begin to express CD160 until day +92 of the follow-up period. Taken together, our data show that CD160 cannot be considered a cytotoxic marker in CMV-specific CD8+ T cells. © 2007 The Author(s).

Author supplied keywords

Cite

CITATION STYLE

APA

Merino, J., Ramírez, N., Moreno, C., Toledo, E., Fernández, M., & Sánchez-Ibarrola, A. (2007). BY55/CD160 cannot be considered a cytotoxic marker in cytomegalovirus- specific human CD8+ T cells. Clinical and Experimental Immunology, 149(1), 87–96. https://doi.org/10.1111/j.1365-2249.2007.03387.x

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free