Transport spin polarization of Ni_xFe_{1-x}: electronic kinematics and band structure

We present measurements of the transport spin polarization of Ni_xFe_{1-x} (0<x<1) using the recently-developed Point Contact Andreev Reflection technique, and compare them with our first principles calculations of the spin polarization for this system. Surpisingly, the measured spin polarization is almost composition-independent. The results clearly demonstrate that the sign of the transport spin polarization does not coincide with that of the difference of the densities of states at the Fermi level. Calculations indicate that the independence of the spin polarization of the composition is due to compensation of density of states and Fermi velocity in the s- and d- bands

The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis

Acknowledgments This work was supported by European Union ALLFUN (FP7/2007 2013, HEALTH-2010-260338) (Fungi in the setting of inflammation, allergy and autoimmune diseases: Translating basic science into clinical practices ‘‘ALLFUN’’) to D.C.I., F.C., C.F., M.G.N., and N.A.R.G. M.G.N and J.Q. were supported by a Vici grant of The Netherlands Organization of Scientific Research (to M.G.N.). M.G.N. was supported by an ERC Consolidator Grant (nr. 310372). N.A.R.G. was also supported by the Wellcome Trust (086827, 075470, 097377, & 101873).Peer reviewedPublisher PD

STAT1 Hyperphosphorylation and Defective IL12R/IL23R Signaling Underlie Defective Immunity in Autosomal Dominant Chronic Mucocutaneous Candidiasis

We recently reported the genetic cause of autosomal dominant chronic mucocutaneous candidiasis (AD-CMC) as a mutation in the STAT1 gene. In the present study we show that STAT1 Arg274Trp mutations in the coiled-coil (CC) domain is the genetic cause of AD-CMC in three families of patients. Cloning and transfection experiments demonstrate that mutated STAT1 inhibits IL12R/IL-23R signaling, with hyperphosphorylation of STAT1 as the likely underlying molecular mechanism. Inhibition of signaling through the receptors for IL-12 and IL-23 leads to strongly diminished Th1/Th17 responses and hence to increased susceptibility to fungal infections. The challenge for the future is to translate this knowledge into novel strategies for the treatment of this severe immunodeficiency