and T.C.M.F. performed all of the retrovirus transductions and confocal microscopy. J.U. developed the PEPCK tetramer and provided advice on its use. N.G. and W.R.H. produced the Plasmodium peptide-MHC I tetramer and helped design the PbT-I cell-killing assays.

In greenhouse experiments, plant growth-promoting rhizobacteria (PGPR) Serratia marcescens NBRI1213 was evaluated for plant growth promotion and biologic control of foot and root rot of betelvine caused by Phytophthora nicotianae. Bacterization of betelvine (Piper betle L.) cuttings with S. marcescens NBRI1213 induced phenylalanine ammonia-lyase, peroxidase, and polyphenoloxidase activities in leaf and root. Qualitative and quantitative estimation of phenolic compounds was done through high-performance liquid chromatography (HPLC) in leaf and root of betelvine after treatment with S. marcescens NBRI1213 and infection by P. nicotianae. Major phenolics detected were gallic, protocatechuic, chlorogenic, caffeic, ferulic, and ellagic acids by comparison of their retention time with standards through HPLC. In all of the treated plants, synthesis of phenolic compounds was enhanced compared with control. Maximum accumulation of phenolics was increased in S. marcescens NBRI1213-treated plants infected with P. nicotianae. In a greenhouse test, bacterization using S. marcescens NBRI1213 decreased the number of diseased plants compared with nonbacterized controls. There were significant growth increases in shoot length, shoot dry weight, root length, and root dry weight, averaging 81%, 68%, 152%, and 290%, respectively, greater than untreated controls. This is the first report of PGPR-mediated induction of phenolics for biologic control and their probable role in protecting betelvine against P. nicotianae, an important soil-borne phytopathogenic fungus.

Graphical Abstract Highlights d Type I IFNs are major upstream regulators of CD4 + T cells from VL patients d Type I IFN signaling-deficient mice have improved control of Leishmania donovani d Type I IFNs inhibit IFNg but promote IL-10-producing antigen-specific CD4 + T cells d Blocking type I IFN signaling enhances anti-parasitic CD4 + T cell responses