DY determinants, possibly associated with novel class II molecules, stimulate autoreactive CD4+ T cells with suppressive activity

A set of T cell clones (TCC) isolated from HLA-DR-, Dw-, DQ-matched allogeneic MLCs was found to proliferate autonomously when stimulated with cells carrying a wide range of class I or II specificities. This apparently unrestricted proliferation was relatively weak, and only low levels of IL-2 were present in the supernatants of stimulated cells. Autologous as well as allogeneic PBMC and B lymphoblastoid cell lines (B-LCL) were capable of stimulating such clones, which were also restimulated by suppressive, but not by helper, TCC. Moreover, such clones displayed the unusual property of autostimulation. mAb inhibition experiments suggested that class II- or class II-restricted antigens were involved in stimulation. Thus, certain "broad" mAbs (TU39, SG520) reacting with multiple locus products inhibited activation of these reagents, but none of those reacting more specifically with DR (TU34, TU37, L243, Q2/70, SG157), DQ (TU22, SPV- L3, Leu 10), or DP (B7/21), or mixtures of these mAbs, were able to do so. Evidence from sequential immunoprecipitation experiments suggested that mAb TU39 bound class II-like molecules other than DR, DQ, and DP on TCC and B-LCL, and it is therefore proposed that such putative novel class II-like molecules may carry the stimulating determinants for these autoreactive clones. DY-reactive clones lacked helper activity for B cells but mediated potent suppressive activity on T cell proliferative responses that was not restricted by the HLA type of the responding cells. Suppressive activity was induced in normal PBMC by such clones, as well as by independent suppressive clones, which was also inhibited only by mAb TU39. These findings lead to the proposal that DY-reactive autostimulatory cells may constitute a self- maintaining suppressive circuit, the level of activity of which would be regulated primarily by the availability of IL-2 in the microenvironmen

Microbial and biochemical changes during the moulding of hay

RESP-498

F2move: fMRI-compatible haptic object manipulation system for closed-loop motor control studies

Functional neuroimaging plays a key role in addressing open questions in systems and motor neuroscience directly applicable to brain machine interfaces. Building on our low-cost motion capture technology (fMOVE), we developed f2MOVE, an fMRI-compatible system for 6DOF goal-directed hand and wrist movements of human subjects enabling closed-loop sensorimotor haptic experiments with simultaneous neuroimaging. f2MOVE uses a high-zoom lens high frame rate camera and a motion tracking algorithm that tracks in real-time the position of special markers attached to a hand-held object in a novel customized haptic interface. The system operates with high update rate (120 Hz) and sufficiently low time delays (<; 20 ms) to enable visual feedback while complex, goal-oriented movements are recorded. We present here both the accuracy of our motion tracking against a reference signal and the efficacy of the system to evoke motor control specific brain activations in healthy subjects. Our technology and approach thus support the real-time, closed-loop study of the neural foundations of complex haptic motor tasks using neuroimaging

Sex differences in gene expression and proliferation are dependent on the epigenetic modifier HP1γ

Summary Sex differences in growth rate in very early embryos have been recognized in a variety of mammals and attributed to sex-chromosome complement effects as they occur before overt sexual differentiation. We previously found that sex-chromosome complement, rather than sex hormones regulates heterochromatin-mediated silencing of a transgene and autosomal gene expression in mice. Here, sex dimorphism in proliferation was investigated. We confirm that male embryonic fibroblasts proliferate faster than female fibroblasts and show that this proliferation advantage is completely dependent upon heterochromatin protein 1 gamma (HP1γ). To determine whether this sex-regulatory effect of HP1γ was a more general phenomenon, we performed RNA sequencing on MEFs derived from males and females, with or without HP1γ. Strikingly, HP1γ was found to be crucial for regulating nearly all sexually dimorphic autosomal gene expression because deletion of the HP1γ gene in males abolished sex differences in autosomal gene expression. The identification of a key epigenetic modifier as central in defining gene expression differences between males and females has important implications for understanding physiological sex differences and sex bias in disease