Importance of Itinerancy and Quantum Fluctuations for the Magnetism in Iron Pnictides

By applying density functional theory, we find strong evidence for an itinerant nature of magnetism in two families of iron pnictides. Furthermore, by employing dynamical mean field theory with continuous time quantum Monte Carlo as an impurity solver, we observe that the antiferromagnetic metal with small magnetic moment naturally arises out of coupling between unfrustrated and frustrated bands. Our results point to a possible scenario for magnetism in iron pnictides where magnetism originates from a strong instability at the momentum vector ($\pi$, $\pi$, $\pi$) while it is reduced by quantum fluctuations due to the coupling between weakly and strongly frustrated bands.Comment: 4 pages, 4 figure

Narrowing the window for millicharged particles by CMB anisotropy

We calculate the cosmic microwave background (CMB) anisotropy spectrum in models with millicharged particles of electric charge q\sim 10^{-6}-10^{-1} in units of electron charge. We find that a large region of the parameter space for the millicharged particles exists where their effect on the CMB spectrum is similar to the effect of baryons. Using WMAP data on the CMB anisotropy and assuming Big Bang nucleosynthesis value for the baryon abundance we find that only a small fraction of cold dark matter, Omega_{mcp}h_0^2 < 0.007 (at 95% CL), may consists of millicharged particles with the parameters (charge and mass) from this region. This bound significantly narrows the allowed range of the parameters of millicharged particles. In models without paraphoton millicharged particles are now excluded as a dark matter candidate. We also speculate that recent observation of 511 keV gamma-rays from the Galactic bulge may be an indication that a (small) fraction of CDM is comprised of the millicharged particles.Comment: 10 pages, 3 figures; v2: journal version, references adde

Nonlinear thermoelectric response of quantum dots: renormalized dual fermions out of equilibrium

The thermoelectric transport properties of nanostructured devices continue to attract attention from theorists and experimentalist alike as the spatial confinement allows for a controlled approach to transport properties of correlated matter. Most of the existing work, however, focuses on thermoelectric transport in the linear regime despite the fact that the nonlinear conductance of correlated quantum dots has been studied in some detail throughout the last decade. Here, we review our recent work on the effect of particle-hole asymmetry on the nonlinear transport properties in the vicinity of the strong coupling limit of Kondo-correlated quantum dots and extend the underlying method, a renormalized superperturbation theory on the Keldysh contour, to the thermal conductance in the nonlinear regime. We determine the charge, energy, and heat current through the nanostructure and study the nonlinear transport coefficients, the entropy production, and the fate of the Wiedemann-Franz law in the non-thermal steady-state. Our approach is based on a renormalized perturbation theory in terms of dual fermions around the particle-hole symmetric strong-coupling limit.Comment: chapter contributed to 'New Materials for Thermoelectric Applications: Theory and Experiment' Springer Series: NATO Science for Peace and Security Series - B: Physics and Biophysics, Veljko Zlatic (Editor), Alex Hewson (Editor). ISBN: 978-9400749863 (2012

S1P1 receptor directs the release of immature B cells from bone marrow into blood

S1P1 receptor expression is required for the egress of newly formed T cells from the thymus and exit of mature T and B cells from secondary lymphoid organs. In this study, we deleted the expression of the S1P1 receptor gene (S1pr1) in developing B cells in the bone marrow. Although B cell maturation within the bone marrow was largely normal in the B cell–specific S1pr1 knockout (B-S1pr1KO) mice, their newly generated immature B cells appeared in the blood at abnormally low numbers as compared with control mice. In the bone marrow of B-S1pr1KO mice, immature B cells in contact with the vascular compartment displayed increased apoptosis as compared with control mice. Forced expression of CD69, a negative regulator of S1P1 receptor expression, in developing bone marrow B cells also reduced the number of immature B cells in the blood. Attenuation of CXCR4 signaling, which is required for the proper retention of developing B cells in bone marrow, did not release immature B cells into the blood of B-S1pr1KO mice as effectively as in control mice. Our results indicate that the S1P1 receptor provides a signal necessary for the efficient transfer of newly generated immature B cells from the bone marrow to the blood

The nuclear orphan receptor Nr4a2 induces Foxp3 and regulates differentiation of CD4+ T cells

Regulatory T cells (Tregs) have a central role in maintaining immune homoeostasis through various mechanisms. Although the Forkhead transcription factor Foxp3 defines the Treg cell lineage and functions, the molecular mechanisms of Foxp3 induction and maintenance remain elusive. Here we show that Foxp3 is one of the direct targets of Nr4a2. Nr4a2 binds to regulatory regions of Foxp3, where it mediates permissive histone modifications. Ectopic expression of Nr4a2 imparts Treg-like suppressive activity to naïve CD4+ T cells by inducing Foxp3 and by repressing cytokine production, including interferon-γ and interleukin-2. Deletion of Nr4a2 in T cells attenuates induction of Tregs and causes aberrant induction of Th1, leading to the exacerbation of colitis. Nr4a2-deficeint Tregs are prone to lose Foxp3 expression and have attenuated suppressive ability both in vitro and in vivo. Thus, Nr4a2 has the ability to maintain T-cell homoeostasis by regulating induction, maintenance and suppressor functions of Tregs, and by repression of aberrant Th1 induction

Resistance to TGFβ suppression and improved anti-tumor responses in CD8⁺ T cells lacking PTPN22

Transforming growth factor β (TGFβ) is important in maintaining self-tolerance and inhibits T cell reactivity. We show that CD8⁺ T cells that lack the tyrosine phosphatase Ptpn22, a major predisposing gene for autoimmune disease, are resistant to the suppressive effects of TGFβ. Resistance to TGFβ suppression, while disadvantageous in autoimmunity, helps Ptpn22‾/‾ T cells to be intrinsically superior at clearing established tumors that secrete TGFβ. Mechanistically, loss of Ptpn22 increases the capacity of T cells to produce IL-2, which overcomes TGFβ-mediated suppression. These data suggest that a viable strategy to improve anti-tumor adoptive cell therapy may be to engineer tumor-restricted T cells with mutations identified as risk factors for autoimmunity

Electronic Structure Calculation by First Principles for Strongly Correlated Electron Systems

Recent trends of ab initio studies and progress in methodologies for electronic structure calculations of strongly correlated electron systems are discussed. The interest for developing efficient methods is motivated by recent discoveries and characterizations of strongly correlated electron materials and by requirements for understanding mechanisms of intriguing phenomena beyond a single-particle picture. A three-stage scheme is developed as renormalized multi-scale solvers (RMS) utilizing the hierarchical electronic structure in the energy space. It provides us with an ab initio downfolding of the global band structure into low-energy effective models followed by low-energy solvers for the models. The RMS method is illustrated with examples of several materials. In particular, we overview cases such as dynamics of semiconductors, transition metals and its compounds including iron-based superconductors and perovskite oxides, as well as organic conductors of kappa-ET type.Comment: 44 pages including 38 figures, to appear in J. Phys. Soc. Jpn. as an invited review pape

Defective IL-10 signaling in hyper-IgE syndrome results in impaired generation of tolerogenic dendritic cells and induced regulatory T cells

Dendritic cells from patients with hyper-IgE syndrome less efficiently generate induced regulatory T cells

Transforming Growth Factor β Signaling Pathway Associated Gene Polymorphisms May Explain Lower Breast Cancer Risk in Western Indian Women

Transforming growth factor β1 (TGFB1) T29C and TGF β receptor type 1 (TGFBR1) 6A/9A polymorphisms have been implicated in the modulation of risk for breast cancer in Caucasian women. We analyzed these polymorphisms and combinations of their genotypes, in pre menopausal breast cancer patients (N = 182) and healthy women (N = 236) from western India as well as in breast cancer patients and healthy women from the Parsi community (N = 48 & 171, respectively). Western Indian women were characterized by a higher frequency of TGFB1*C allele of the TGF β T29C polymorphism (0.48 vs 0.44) and a significantly lower frequency of TGFBR1*6A allele of the TGFBR1 6A/9A polymorphism (0.02 vs 0.068, p<0.01) as compared to healthy Parsi women. A strong protective effect of TGFB1*29C allele was seen in younger western Indian women (<40 yrs; OR = 0.45, 95% CI 0.25–0.81). Compared to healthy women, the strikingly higher frequencies of low or intermediate TGF β signalers in patients suggested a strong influence of the combination of these genotypes on the risk for breast cancer in Parsi women (for intermediate signalers, OR = 4.47 95%CI 1.01–19.69). The frequency of low signalers in Parsi healthy women, while comparable to that reported in Europeans and Americans, was three times higher than that in healthy women from western India (10.6% vs 3.3%, p<0.01). These observations, in conjunction with the low incidence rate of breast cancer in Indian women compared to White women, raise a possibility that the higher frequency of TGFB1*29C allele and lower frequency of TGFBR1*6A allele may represent important genetic determinants that together contribute to a lower risk of breast cancer in western Indian women

Immunophenotyping of Circulating T Helper Cells Argues for Multiple Functions and Plasticity of T Cells In Vivo in Humans - Possible Role in Asthma

BACKGROUND: The immune process driving eosinophilic and non-eosinophilic asthma is likely driven by different subsets of T helper (Th) cells. Recently, in vitro studies and animal studies suggest that Th cell subsets displays plasticity by changing their transcription factor or by expressing multiple transcription factors. Our aim was to determine whether individuals with asthma and elevated circulating eosinophils express signs of different regulatory immune mechanisms compared with asthmatics with low blood eosinophils and non-asthmatic control subjects. In addition, determine the relationship between eosinophilia and circulating Th cell subsets. METHODOLOGY/PRINCIPAL FINDINGS: Participants were selected from a random epidemiological cohort, the West Sweden Asthma Study. Immunophenotypes of fresh peripheral blood cells obtained from stable asthmatics, with and without elevated eosinophilic inflammation (EOS high and EOS low respectively) and control subjects, were determined by flow cytometry. No differences in the number of Th1 (T-bet), Th2 (GATA-3), Th17 (RORγt) or Treg (FOXP3) cells were observed between the groups when analysing each subset separately. However, in all groups, each of the Th subsets showed expression of additional canonical transcription factors T-bet, GATA-3, RORγt and FOXP3. Furthermore, by in vitro stimulation with anti-CD3/anti-CD28 there was a significant increase of single expressing GATA-3(+) and co-expressing T-bet(+)GATA-3(+) cells in the EOS high asthmatics in comparison with control subjects. In addition, T-bet(-)GATA-3(+)RORγt(+)FOXP3(+) were decreased in comparison to the EOS low asthmatics. Finally, in a group of control subjects we found that the majority of proliferating Th cells (CD4(+)CD25(+)Ki67(+)) expressed three or four transcription factors. CONCLUSIONS: The ability of human Th cells to express several regulatory transcription factors suggests that these cells may display plasticity in vivo