CD8 lymphocytosis in primary cytomegalovirus (CMV) infection of allograft recipients: expansion of an uncommon CD8+ CD57− subset and its progressive replacement by CD8+CD57+ T cells
Allograft recipients undergoing eytomegalovirus infection present increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and five liver allograft recipients with primary CMV infection but no other etiological factor of graft dysfunction revealed selective imbalances of peripheral blood CDS+ T cell subsets. Initially, CMV viraemia is associated with elevated CDS+ bright T cell numbers and T cell activation. Activation markers fall to normal when viral cultures become negative (before the end of the first month). During the second to sixth month, most (12/16) patients keep up high CD8+ T cell counts (1050‐2900 CD8+ cells/mm3), comprising an uncommon CD8+ T cell subset, as 45‐73% of CD8+bright lymphocytes were CD3+ and TCRαβ+, but were not stained by anti‐CD28, CDIIb, CD16. CD56. and CD57 antibody. Unexpectedly, CD8+CD57+ T cells, a hallmark of CMV infection, do not appear until the second to sixth month of primary CMV infection, and their numbers increase progressively thereafter. They become the predominant CD8+ T cell subset after 6 months of infection and their persistence for several (up to 4) years is strongly correlated (r = 0‐87) with expansion of CD8+ cells. By analysis with MoAbs, there was no bias towards the use of particular TCR‐Vβ gene families al any time of primary CMV infection. Persistence of CD8 lymphocytosis is thus directly related to the rate of expansion of an uncommon CD8+ CD57‐ subset and its progressive replacement by CD8+ CD57+ T cells that are chronically elicited by CMV.