Signals orchestrating productive CD4⁺ T‐cell responses are well documented; however, the regulation of contraction of CD4⁺ T‐cell effector populations following the resolution of primary immune responses is not well understood. While distinct mechanisms of T‐cell death have been defined, the relative importance of discrete death pathways during the termination of immune responses in vivo remains unclear. Here, we review the current understanding of cell‐intrinsic and ‐extrinsic variables that regulate contraction of CD4⁺ T‐cell effector populations through multiple pathways that operate both initially during T‐cell priming and later during the effector phase. We discuss the relative importance of antigen‐dependent and ‐independent mechanisms of CD4⁺ T‐cell contraction during in vivo responses, with a special emphasis on influenza virus infection. In this model, we highlight the roles of greater differentiation and presence in the lung of CD4⁺ effector T cells, as well as their polarization to particular T‐helper subsets, in maximizing contraction. We also discuss the role of autocrine interleukin‐2 in limiting the extent of contraction, and we point out that these same factors regulate contraction during secondary CD4⁺ T‐cell responses.