IL2 and Sepsis: This increased vulnerability is partly due to impaired T-cell responses in septic hosts, leading to a reduced number of effector CD8 + T cells capable of producing key effector cytokines, such as IFN-γ, TNF-α, and IL-2.[62,63] Our study also confirms that a higher proportion of Effector Memory CD8 + T cells serves as a protective factor against sepsis.