Lymphocytes must circulate from blood into lymphoid tissues and sites of infection and inflammation to function efficiently in vivo. This process of “homing” is in part directed by the expression of the leukocyte adhesion molecule (LAM‐1, also known as TQ1 and Leu‐8) in humans and the homologous MEL‐14 antigen in mice. In this report, we demonstrate that the LAM‐1 molecule is a 74‐kDaprotein and that only half of the CD4⁺ T cells in humans which have a memory phenotype (CD45RA ⁻CD29^hi) express the LAM‐1 molecule. Functionally, these two phenotypically distinct subpopulations of memory cells were quite different. The LAM‐1⁺ memory cells proliferated better to recall antigen and induced three to seven times higher levels of B cell immunoglobulin secretion than their LAM‐1⁻ counterparts. Thus, antigen‐specific memory T cellswithin the helper lineage express the homing receptor appropriate for regulating their migration to secondary lymphoid tissues and sites of inflammation.