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According to a popular quip, fittingly though incorrectly attributed to the great dyspeptic metaphysicist Arthur Schopenhauer, all truth passes through three stages: first, it is ridiculed; second, it is violently opposed; third, it is accepted as self-evident (1). In the iconoclastic world of biomedical research, however, that is so eager to challenge the old and propose novel paradigms, the evolution of truth may at times take a different path, traveling the route to knowledge almost in the opposite direction: first, a discovery is excitedly embraced; second, it is readily confirmed and expanded upon; and third, it is effectively contested and quietly slips into oblivion. That, or so it seemed, was to be the fate of the chemokine CXCL10 and its receptor CXCR3 as promising therapeutic targets in type 1 diabetes (T1D). Yet in this issue of Diabetes , Lasch et al. (2) pull that concept back from the brink by defining a specific context for effective CXCL10 neutralization, namely, as an adjunct treatment to achieve durable aCD3-induced T1D remission.In the early 2000s, buoyed by a burgeoning interest in the potential contribution of individual chemokine/receptors to diabetes development, two independent groups studying the virus-induced RIP-LCMV-GP model suggested that the CXCL10:CXCR3 axis might constitute a key determinant for T1D pathogenesis (3,4). Transgenic RIP-LCMV-GP mice, in which the rat insulin promoter (RIP) drives expression of the lymphocytic choriomeningitis virus (LCMV) glycoprotein (GP) specifically in β-cells, are phenotypically normal but readily develop T1D within ∼2 weeks after LCMV infection and the generation of a potent LCMV-GP–specific CD8+T-cell response. Based on mRNA and protein expression screens of murine islets or pancreata obtained from infected RIP-LCMV-GP mice, CXCL10 was identified as a particularly prominent chemokine (3,4), and corresponding in vivo …

Back From the Brink: The Uses of Targeting the CXCL10:CXCR3 Axis in Type 1 Diabetes