CD4(+)CD7(-) T cells: A separate subpopulation of memory T cells?

The CD7 molecule is apparently involved in T cell activation but is absent in a substantial subpopulation of human T cells under physiological and certain pathological conditions. The majority of CD7(-) T cells expresses TCR alpha/beta and is of CD4(+) helper and CD45R0(+)CD45RA(-) memory phenotype. After birth, percentages and absolute numbers of circulating CD7(-) T cells increase significantly during aging. A number of molecules thought to be involved in organ-specific T cell homing are preferentially expressed within the subset of CD4(+)CD7(-) T cells. Specific absence of CD7 antigen expression on T cells is observed in a variety of pathologic conditions such as cutaneous T cell lymphoma, HIV infection, rheumatoid arthritis, and kidney transplantation. Current in vitro results suggest that specific downregulation of CD7 antigen expression in T cells reflects a separate and stable differentiation state occurring late in the immune response. Expansion of CD7(-) T cells in vivo has been found in certain diseases associated with chronically repeated T cell stimulation. The potential pathophysiological significance of this T cell subset in certain human diseases is discussed.