The adaptive immune response, particularly T cell responses, plays a crucial role in the clinical outcome of SARS-CoV-2 infection and vaccine efficacy. T cells develop early and correlate with protection, but are impaired in severe disease and associated with lymphopenia. A subset of T cells primed against seasonal coronaviruses cross-reacts with SARS-CoV-2, contributing to clinical protection, especially in early life. T cell memory is broad, recognizing around 30 epitopes per individual, and is well-sustained. This breadth limits the impact of viral mutations and underpins protection against severe disease, including from variants like Omicron. Current COVID-19 vaccines elicit robust T cell responses, contributing to protection against hospitalization and death. T cell immunity is central to controlling SARS-CoV-2, and its importance may have been underestimated. The cellular immune response, essential for controlling intracellular pathogens, evolved to recognize and control SARS-CoV-2, with T cells being the major mediators of disease control. Studies on T cell responses against SARS-CoV-2 show that they are strong in severe infections, with early and robust interferon and adaptive immune responses controlling viral load. Lymphopenia is common in acute SARS-CoV-2 infection, and the functional capacity of the cellular response is a key determinant of clinical outcome. T cell responses are also elicited after vaccination, contributing to protection against severe disease and death. The magnitude and quality of T cell responses vary with vaccine type and history of prior infection, and new formulations are being developed to enhance cellular responses. T cell responses are critical for preventing initial infection and limiting disease severity, and they may underpin the outstanding protection against severe infection and death provided by current vaccines. Despite progress, many questions remain about the optimal coordinated cellular response and the role of pre-existing HCoV-specific repertoire in protection. Further research is needed to optimize vaccine formulations and understand how cellular responses contribute to protection against emerging viral variants.The adaptive immune response, particularly T cell responses, plays a crucial role in the clinical outcome of SARS-CoV-2 infection and vaccine efficacy. T cells develop early and correlate with protection, but are impaired in severe disease and associated with lymphopenia. A subset of T cells primed against seasonal coronaviruses cross-reacts with SARS-CoV-2, contributing to clinical protection, especially in early life. T cell memory is broad, recognizing around 30 epitopes per individual, and is well-sustained. This breadth limits the impact of viral mutations and underpins protection against severe disease, including from variants like Omicron. Current COVID-19 vaccines elicit robust T cell responses, contributing to protection against hospitalization and death. T cell immunity is central to controlling SARS-CoV-2, and its importance may have been underestimated. The cellular immune response, essential for controlling intracellular pathogens, evolved to recognize and control SARS-CoV-2, with T cells being the major mediators of disease control. Studies on T cell responses against SARS-CoV-2 show that they are strong in severe infections, with early and robust interferon and adaptive immune responses controlling viral load. Lymphopenia is common in acute SARS-CoV-2 infection, and the functional capacity of the cellular response is a key determinant of clinical outcome. T cell responses are also elicited after vaccination, contributing to protection against severe disease and death. The magnitude and quality of T cell responses vary with vaccine type and history of prior infection, and new formulations are being developed to enhance cellular responses. T cell responses are critical for preventing initial infection and limiting disease severity, and they may underpin the outstanding protection against severe infection and death provided by current vaccines. Despite progress, many questions remain about the optimal coordinated cellular response and the role of pre-existing HCoV-specific repertoire in protection. Further research is needed to optimize vaccine formulations and understand how cellular responses contribute to protection against emerging viral variants.