Signatures of Chiral Dynamics in Low Energy Compton Scattering off the Nucleon

We present a projector formalism which allows to define dynamical polarizabilities of the nucleon from a multipole expansion of the nucleon Compton amplitudes. We give predictions for the energy dependence of these dynamical polarizabilities both from dispersion theory and from leading-one-loop chiral effective field theory. Based on the good agreement between the two theoretical frameworks, we conclude that the energy dependence of the dynamical polarizabilities is dominated by chiral dynamics, except in those multipole channels where the first nucleon resonance Delta(1232) can be excited. Both the dispersion theory framework and a chiral effective field theory with explicit Delta(1232) degrees of freedom lead to a very good description of the available low energy proton Compton data. We discuss the sensitivity of the proton Compton cross section to dynamical polarizabilities of different multipole content and present a fit of the static electric and magnetic dipole polarizabilities from low-energy Compton data up to omega=170 MeV, finding alpha_E=(11.04+-1.36)*10^(-4) fm^3, beta_M =(2.76-+1.36)*10^(-4) fm^3.Comment: 43 pages, 13 figure

IRF4 transcription factor-dependent CD11b+ dendritic cells in human and mouse control mucosal IL-17 cytokine responses.

Mouse and human dendritic cells (DCs) are composed of functionally specialized subsets, but precise interspecies correlation is currently incomplete. Here, we showed that murine lung and gut lamina propria CD11b+ DC populations were comprised of two subsets: FLT3- and IRF4-dependent CD24(+)CD64(-) DCs and contaminating CSF-1R-dependent CD24(-)CD64(+) macrophages. Functionally, loss of CD24(+)CD11b(+) DCs abrogated CD4+ T cell-mediated interleukin-17 (IL-17) production in steady state and after Aspergillus fumigatus challenge. Human CD1c+ DCs, the equivalent of murine CD24(+)CD11b(+) DCs, also expressed IRF4, secreted IL-23, and promoted T helper 17 cell responses. Our data revealed heterogeneity in the mouse CD11b+ DC compartment and identifed mucosal tissues IRF4-expressing DCs specialized in instructing IL-17 responses in both mouse and human. The demonstration of mouse and human DC subsets specialized in driving IL-17 responses highlights the conservation of key immune functions across species and will facilitate the translation of mouse in vivo findings to advance DC-based clinical therapies

Human fetal dendritic cells promote prenatal T-cell immune suppression through arginase-2.

During gestation the developing human fetus is exposed to a diverse range of potentially immune-stimulatory molecules including semi-allogeneic antigens from maternal cells, substances from ingested amniotic fluid, food antigens, and microbes. Yet the capacity of the fetal immune system, including antigen-presenting cells, to detect and respond to such stimuli remains unclear. In particular, dendritic cells, which are crucial for effective immunity and tolerance, remain poorly characterized in the developing fetus. Here we show that subsets of antigen-presenting cells can be identified in fetal tissues and are related to adult populations of antigen-presenting cells. Similar to adult dendritic cells, fetal dendritic cells migrate to lymph nodes and respond to toll-like receptor ligation; however, they differ markedly in their response to allogeneic antigens, strongly promoting regulatory T-cell induction and inhibiting T-cell tumour-necrosis factor-α production through arginase-2 activity. Our results reveal a previously unappreciated role of dendritic cells within the developing fetus and indicate that they mediate homeostatic immune-suppressive responses during gestation