On the phase structure and thermodynamics of QCD

We discuss the phase structure and thermodynamics of QCD by means of dynamical chiral effective models. Quark and meson fluctuations are included via the functional renormalization group. We study the influence of confinement in addition to the impact of fluctuations by comparing the results of the chiral models to their Polyakov-loop extended versions. Furthermore, we discuss the mass sensitivity of the phase structure and thermodynamics and find interesting modifications close to the chiral limit.Comment: 13 pages, 11 figures; Appendix added; published versio

Thermodynamics of QCD at vanishing density

We study the phase structure of QCD at finite temperature within a Polyakov-loop enhanced quark-meson model. Such a model describes the chiral as well as the confinement-deconfinement dynamics. In the present investigation, based on the approach and results put forward in [1-4], both, matter as well as glue fluctuations are included. We present results for the order parameters as well as some thermodynamic observables and find very good agreement with recent results from lattice QCD.Comment: 12 pages, 7 figures; published versio

Exploring the Phase Structure and Thermodynamics of QCD

We put forward a Polyakov-loop extended quark meson model, where matter as well as glue fluctuations are taken into account, cf. [1]. The latter are included via a Polyakov-loop potential. Usually such a glue potential is based on Yang-Mills lattice data only. We show that a parametrisation of unquenching effects as proposed in [2], together with the inclusion of fluctuations via the functional renormalisation group [3,4], accounts for the relevant dynamics. This is demonstrated by a comparison of order parameters and thermodynamic observables to recent lattice results at vanishing chemical potential, where we find very good agreement.Comment: 11 pages, 2 figures, contribution to "QCD-TNT-III: From quarks and gluons to hadronic matter: A bridge too far?", ECT*, Trento (Italy), September 2-6, 201

Antibodies and IL-3 support helminth-induced basophil expansion

Basophils are powerful mediators of Th2 immunity and are present in increased numbers during allergic inflammation and helminth infection. Despite their ability to potentiate Th2 immunity the mechanisms regulating basophil development remain largely unknown. We have found a unique role for isotype-switched antibodies in promoting helminth-induced basophil production following infection of mice with Heligmosomoides polygyrus bakeri or Nippostrongylus brasiliensis. H. polygyrus bakeri-induced basophil expansion was found to occur within the bone marrow, and to a lesser extent the spleen, and was IL-3 dependent. IL-3 was largely produced by CD4+CD49b+NK1.1− effector T cells at these sites, and required the IL-4Rα chain. However, antibody-deficient mice exhibited defective basophil mobilization despite intact T-cell IL-3 production, and supplementation of mice with immune serum could promote basophilia independently of required IL-4Rα signaling. Helminth-induced eosinophilia was not affected by the deficiency in isotype-switched antibodies, suggesting a direct effect on basophils rather than through priming of Th2 responses. Although normal type 2 immunity occurred in the basopenic mice following primary infection with H. polygyrus bakeri, parasite rejection following challenge infection was impaired. These data reveal a role for isotype-switched antibodies in promoting basophil expansion and effector function following helminth infection

The phase structure of the Polyakov--quark-meson model beyond mean field

The Polyakov-extended quark-meson model (PQM) is investigated beyond mean-field. This represents an important step towards a fully dynamical QCD computation. Both the quantum fluctuations to the matter sector and the back-reaction of the matter fluctuations to the QCD Yang-Mills sector are included. Results on the chiral and confinement-deconfinement crossover/phase transition lines and the location of a possible critical endpoint are presented. Moreover, thermodynamic quantities such as the pressure and the quark density are discussed.Comment: 12 pages, 11 figure

TLR and RLR signaling are reprogrammed in opposite directions after detection of viral infection

Innate immune recognition of RNA is key for the initiation of immunity in response to viral infection. Although the factors controlling the detection of viral RNA by innate immune receptors in host cells are increasingly well understood, little is known about the dynamic changes in signaling after the initial triggering of these receptors. In this study, we report that preconditioning with the synthetic dsRNA polyinosinic-polycytidylic acid [poly(I:C)], a mimetic of viral RNA, rapidly reprograms murine APCs by simultaneously augmenting sensitivity of endosomal TLRs and inhibiting activation of RIG-I–like receptors (RLRs) in an IFN-β–dependent manner. These changes in receptor sensitivity were also seen in vivo after treatment of mice with poly(I:C). Mechanistically, the increased sensitivity of the TLR pathway was associated with elevated MAPK and NF-κB activity. The RLR response was inhibited downstream of TANK-binding kinase-1, resulting in decreased IFN regulatory factor 3 phosphorylation. Reprogramming of pattern-recognition receptor signaling also occurred after viral infection, because infection of host cells with Sendai virus or their exposure to supernatant from virus-infected cells induced the same changes in TLR and RLR sensitivity as poly(I:C). Thus, innate recognition of viral infection critically modifies responses to pattern-recognition receptor stimulation. These dynamic adaptations to infection may reinforce antiviral immunity and at the same time serve to limit pathological inflammation

Reprogramming of TLR7 signaling enhances antitumor NK and cytotoxic T cell responses

Toll-like receptor (TLR) 7 agonists are effective in topical application for the immunotherapy of skin cancers, but their performance for the systemic treatment of solid tumors is limited by the development of TLR tolerance. In this study, we describe a novel strategy to overcome TLR tolerance and enhance TLR7-dependent antitumor immune responses through reprogramming of TLR signaling pathways. The sensitivity of TLR7 signaling in dendritic cells (DC) was increased by prior stimulation with the dsRNA poly(I:C) that mimics virally induced immune activation. Timing of the stimulations was important, as sequential stimulation with poly(I:C) and the TLR7 agonist R848 interspaced by 24 h induced higher MAPK and NFkB signaling in DC than the simultaneous application of the same ligands. DC activated by sequential poly(I:C)/R848 stimulation efficiently induced Th1 differentiation and primed NK-cell and cytotoxic T-cell responses. We have developed a treatment regimen taking advantage of TLR7 reprogram-ming that cured over 80% of large immunogenic tumors in mice by the action of NK cells and cytotoxic T cells. These results have direct implications for the use of these clinically established ligands in the immunotherapy of cancer