We present results for the isospin-0 ππ s-wave scattering length calculated with Osterwalder-Seiler valence quarks on Wilson twisted mass gauge configurations. We use three N f = 2 ensembles with unitary (valence) pion mass at its physical value (250 MeV), at 240 MeV (320 MeV) and at 330 MeV (400 MeV), respectively. By using the stochastic Laplacian Heaviside quark smearing method, all quark propagation diagrams contributing to the isospin-0 ππ correlation function are computed with sufficient precision. The chiral extrapolation is performed to obtain the scattering length at the physical pion mass.Our result M π a I=0 0 = 0.198(9)(6) agrees reasonably well with various experimental measurements and theoretical predictions. Since we only use one lattice spacing, certain systematics uncertainties, especially those arising from unitary breaking, are not controlled in our result.

We present results for the interaction of two kaons at maximal isospin. The calculation is based on N f = 2 + 1 + 1 flavour gauge configurations generated by the European Twisted Mass Collaboration with pion masses ranging from about 230 MeV to 450 MeV at three values of the lattice spacing. The elastic scattering length a I=1 0 is calculated at several values of the bare strange and light quark masses. We find M K a 0 = −0.385(16) stat ( +0 −12 ) ms ( +0 −5 ) Z P (4) r f as the result of a combined extrapolation to the continuum and to the physical point, where the first error is statistical, and the three following are systematical. This translates to a 0 = −0.154(6) stat ( +0 −5 ) ms ( +0 −2 ) Z P (2) r f fm.1 arXiv:1703.04737v2 [hep-lat]

SUMMARYAbsence of CD7 is a stable phenotype in a subset of normal human T cells. Most circulating CD7 ÿ T cells express the CD4CD45RO CD45RA ÿ memory phenotype. We analysed CD4 CD45RA ÿ peripheral blood lymphocytes that were separated into CD7 and CD7 ÿ for their in vitro cytokine secretion in response to different stimuli. The CD4 + CD7 -subpopulation was found to secrete significantly higher levels of IL-5 compared with the CD4 + CD7 + subset upon stimulation with ionomycin/phorbol myristate acetate (PMA) plus anti-CD28 MoAbs. In contrast to IL-5 secretion, IL-4 and interferon-gamma (IFN-°) secretion was not significantly different in CD7 and CD7 ÿ T cells upon stimulation in vitro. The data indicate that the CD4 CD7 ÿ T cell represents the majority of IL-5-secreting cells within the population of CD4 CD45RA ÿ memory T cells. Since CD4 CD7 ÿ T cells were found to be enriched in various skin lesions associated with eosinophilic infiltration, the results of our study support the hypothesis that skin-infiltrating CD7 ÿ T cells are one of the major sources of IL-5 responsible for the development of eosinophilic inflammation in certain skin diseases.

SUMMARYDirected migration of lymphocytes from blood into lymph nodes and organ-associated lymphatic tissue, also referred to as homing, is initiated by T-cell adhesion to specialized high endothelial cells of postcapillary vessels. Here, we demonstrate that selective signal transduction pathways specifically modulate the expression of the cutaneous lymphocyte antigen (CLA), the putative skin-homing receptor, during naive to memory transition of CD4+ T cells in vitro. The results show that the expression of CLA is strongly induced by activation via CD2 [TI 1.1 + T11.2 monoclonal antibodies (mAb)]. Addition of transforming growth factor-fil (TGF-PI), interleukin-6 (IL-6), and, to a lesser extent, IL-2 further enhanced the generation of CLA+ T cells, whereas the induction of this antigen was markedly inhibited by IL-4. Periodic restimulation via CD2 and long-term culture of activated cells in the presence of IL-2 and TGF-BI resulted in stable expression of CLA during a culture period of more than 100 days. In contrast, activation of naive CD4+ T cells via CD3, CD28 or by mitogens induced a rapid naive to memory phenotype transition but a much lower percentage of CLA+ T cells showing only weak expression of the antigen. Furthermore, activation of purified CD4+ memory T cells by CD2 strongly induced expression of activation-related antigens CD25 and HLA-DR, but failed to up-regulate CLA expression. Our results show that primary stimulation conditions highly modulate the development of skin-associated T cells and indicate a new functional role for costimulatory adhesion pathways in regulating the expression of molecules associated with T-cell homing.