Abstract The thymus is the primary site of T cell development, generating a diverse repertoire of T cells that protects us from various threats. Despite its crucial role in T cell immunity, the thymus undergoes chronic involution that leads to a decline in T cell production and impaired T cell immunity. Although the thymus is highly sensitive to various forms of damage, and everyday insults like stress and infection, it also has a remarkable capacity to regenerate itself. Though this reparative capacity declines with age. We hypothesized that age-related thymic decline may be attributed to repeated damage and regeneration cycles in response to everyday insults. We expected impaired regeneration with each round of damage. However, we found that after three rounds of damage and repair cycles, overall thymic cellularity consistently returned to homeostasis. Moreover, we also found that unlike injury from ionizing radiation, Dexamethasone (Dex) mediated damage led to thymic hypertrophy. Preliminary studies revealed that type 2 cytokines, previously implicated to promote thymic regeneration, are elevated in the early phases of Dex induced damage, but not during irradiation. Comparing thymic cellularity between damage models, we found that Dex induced damage had faster recovery kinetics and led to thymic hypertrophy 28 days after damage. We hypothesize that type 2 immunity may be a key contributor to hypertrophic thymic regeneration in Dex induced thymic damage. We will test our hypothesis through genetic mouse models, cytokine modulation, and standard immunophenotyping. The positive results of this study will augment our basic knowledge of the endogenous mechanisms of thymic regeneration and inform the creation of thymic boosting therapies. I am supported in part by PHS NRSA T32GM007270 from NIGMS.