D’Acquisto et al. (2007b) investigated the effect of AnxA1 on T cell differentiation and observed that exogenous AnxA1 favored generation of the IFNγ-producing Th1 subset, while inhibiting development of the IL-4-producing Th2 subset. To test if this subset “skewing” also occurred in vivo, they examined the Th1-dominant collagen-induced model of arthritis (CIA) and observed that exogenously administered AnxA1 induced exacerbation of joint inflammation associated with increased lymphocyte production of the key Th1 cytokine, IFN-γ. Here, IFNG is linked to arthritic joint disease.