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Bcl6 Acts as an Amplifier for the Generation and Proliferative Capacity of Central Memory CD8⁺ T Cells¹

Hirohito Ichii^2,*,, Akemi Sakamoto^*, Yoshikazu Kuroda and Takeshi Tokuhisa^3,*

^* Department of Developmental Genetics, Graduate School of Medicine, Chiba University, Chiba, Japan; and Department of Gastrointestinal Surgery, Graduate School of Medical Sciences, Kobe University, Kobe, Japan

Central memory CD8⁺ T cells (T_CM) are considered to be more efficient than effector ones (T_EM) for mediating protective immunity. The molecular mechanism involved in the generation of these cells remains elusive. Because Bcl6 plays a role in the generation and maintenance of memory CD8⁺ T cells, we further examined this role in the process in relation to T_CM and T_EM subsets. In this study, we show that T_CM and T_EM were functionally identified in CD62L⁺ and CD62L^– memory (CD44⁺Ly6C⁺) CD8⁺ T cell subsets, respectively. Although T_CM produced similar amounts of IFN- and IL-2 to T_EM after anti-CD3 stimulation, the cell proliferation capacity after stimulation and tissue distribution profiles of T_CM differed from those of T_EM. Numbers of T_CM were greatly reduced and elevated in spleens of Bcl6-deficient and lck-Bcl6 transgenic mice, respectively, and those of T_EM were constant in nonlymphoid organs of these same mice. The majority of Ag-specific memory CD8⁺ T cells in spleens of these mice 10 wk after immunization were T_CM, and the number correlated with Bcl6 expression in T cells. The proliferation of Ag-specific memory CD8⁺ T cells upon secondary stimulation was dramatically up-regulated in lck-Bcl6 transgenic mice, and the adoptive transfer experiments with Ag-specific naive CD8⁺ T cells demonstrated that some of the up-regulation was due to the intrinsic effect of Bcl6 in the T cells. Thus, Bcl6 is apparently a crucial factor for the generation and secondary expansion of T_CM.

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