Acute Kidney Injury (AKI), when left untreated, transitions into chronic kidney disease (CKD). The role of CD4 + T lymphocytes has long been associated with determining the disease fate due to their ability to modulate the immune response by releasing cytokines and assisting the actions of CD8 + T lymphocytes, macrophages and aiding in the secretion of immunoglobulins by B cells. In this review, we focus on the roles of Th1, Th2, Th9, Th17, Th22, and TFH cells and the signaling cascades driving AKI progression, resolution, and cell death. Murine models have been pivotal in elucidating pro- and anti-inflammatory cytokine modulation. Diagnosing AKI requires potent biomarkers to assess disease severity and outcomes, which, coupled with immunological insights, could improve AKI treatment and reduce mortality. This review provides a roadmap of immune dynamics from AKI onset through resolution and related cell death events.