Interleukin-2 (IL-2), a cytokine, is crucial for immune homeostasis. It impacts regulatory T (Treg) cells and fine-tunes effector lymphocyte responses [1]. IL-2 was first identified as a growth factor driving the expansion of activated human T cell populations, and its expression, receptor signaling, and biological actions have been extensively studied over the past 40 years [2]. It is involved in regulating CD4+ T cell differentiation and function, as well as the effector and memory responses of CD8+ T cells [2].

In a mouse model of chikungunya virus-induced arthritis, treatment with an IL-2/anti-IL-2 complex increased both Tregs and effector (Teff) T cells, without significantly reducing inflammation or disease scores, while the anti-IL-2 mAb alone, which moderately increased IL-2 levels and activated Tregs, decreased the average disease score. This indicates complex immune-modulating effects of IL-2 in this disease context [3,4]. Mathematical models have also been developed to study the impact of IL-2 modulation therapies on T cell dynamics, simulating the effects of different treatments such as injection of IL-2, anti-IL-2 antibodies, IL-2/anti-IL-2 immune-complexes, and mutant variants of IL-2 to understand the dose and timing conditions for promoting either immunity or tolerance [5].

In conclusion, IL-2 is a key cytokine in immune regulation, with its actions affecting T cell differentiation, function, and immune responses. Mouse models, such as those for chikungunya-induced arthritis, and mathematical models have provided insights into its role in disease and potential therapeutic applications. These studies help in understanding how to manipulate IL-2's actions for treating autoimmune diseases and cancer [1,2,3,4,5].