T cells, particularly CD8⁺ T cells, are major participants in obesity-linked adipose tissue (AT) inflammation. We examined the mechanisms of CD8⁺ T-cell accumulation and activation in AT and the role of CD11a, a β2 integrin.

CD8⁺ T cells in AT of obese mice showed activated phenotypes with increased proliferation and interferon-γ expression. In vitro, CD8⁺ T cells from mouse AT displayed increased interferon-γ expression and proliferation to stimulation with interleukin-12 and interleukin-18, which were increased in obese AT. CD11a was upregulated in CD8⁺ T cells in obese mice. Ablation of CD11a in obese mice dramatically reduced T-cell accumulation, activation, and proliferation in AT. Adoptive transfer showed that CD8⁺ T cells from wild-type mice, but not from CD11a-deficient mice, infiltrated into AT of recipient obese wild-type mice. CD11a deficiency also reduced tumor necrosis factor-α–producing and interleukin-12–producing macrophages in AT and improved insulin resistance.

Combined action of cytokines in obese AT induces proliferative response of CD8⁺ T cells locally, which, along with increased infiltration, contributes to CD8⁺ T-cell accumulation and activation in AT. CD11a plays a crucial role in AT inflammation by participating in T-cell infiltration and activation.