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A facile and universal route for synthesizing transition metal borides has been developed by reaction of boron triiodide (BI 3 ) with elemental transition metals. This method employs relatively low synthesis temperatures to afford single-phase samples of various binary and ternary metal borides, such as Fe 2 B, Co 2 B, Ni 3 B, TiB 2 , VB 2 , CrB 2 , and Ni 2 CoB. This synthesis protocol can be utilized for the topotactic transformation of metal shapes into their respective borides, as exemplified by transformation of Ni foam to Ni 3 B foam. In situ powder X-ray diffraction studies of the Ni–BI 3 system showed that the crystalline nickel borides, Ni 4 B 3 and Ni 2 B, start to form at temperatures as low as 700 K and 877 K, respectively, which is significantly lower than the typical synthesis temperatures required to produce these borides. Ni 3 B synthesized by this method was tested as a supporting material for oxygen evolution reaction (OER) in acidic media. Composite electrocatalysts of IrO 2 /Ni 3 B with only 50% of IrO 2 exhibit current densities and stability similar to pure IrO 2 at mass loadings lower than 0.5 mg cm −2 , indicating Ni 3 B could be a promising supporting material for acidic OER. 

Besides the central role of classical Major Histocompatibility Complex (MHC) class Ia-restricted conventional Cluster of Differentiation 8 (CD8) T cells in antiviral host immune response, the amphibian Xenopus laevis critically rely on MHC class I-like (mhc1b10.1.L or XNC10)-restricted innate-like (i)T cells (iVα6 T cells) to control infection by the ranavirus Frog virus 3 (FV3). To complement and extend our previous reverse genetic studies showing that iVα6 T cells are required for tadpole survival, as well as for timely and effective adult viral clearance, we examined the conditions and kinetics of iVα6 T cell response against FV3. Using a FV3 knock-out (KO) growth-defective mutant, we found that upregulation of the XNC10 restricting class I-like gene and the rapid recruitment of iVα6 T cells depend on detectable viral replication and productive FV3 infection. In addition, by in vivo depletion with XNC10 tetramers, we demonstrated the direct antiviral effector function of iVα6 T cells. Notably, the transitory iV6 T cell defect delayed innate interferon and cytokine gene response, resulting in long-lasting negative inability to control FV3 infection. These findings suggest that in Xenopus and likely other amphibians, an immune surveillance system based on the early activation of iT cells by non-polymorphic MHC class-I like molecules is important for efficient antiviral immune response.