VISTA, a novel mouse Ig superfamily ligand that negatively regulates T cell responses

VISTA suppresses T cell proliferation and cytokine production and can influence autoimmunity and antitumor responses in mice

Mobile laser scanning of linear objects

Mobilne skanowanie laserowe to nowoczesna technologia pozwalająca na zbieranie danych wzdłuż dróg, torów i tuneli bez konieczności wstrzymywania ruchu. Dokładności pomiarów uzyskiwane tą technologią są na poziomie kilku centymetrów, a czas realizacji projektu jest krótszy. W Polsce świadomość korzyści wynikających z zastosowania tej technologii jest wciąż niska.Mobile laser scanning is a new technology allowing to acquire spatial data along the roads, tracks and tunnels without jamming the traffic. Accuracy is few cm and project duration is shorter. In Poland there is still low awareness of the benefits of this technology

Mast cell degranulation breaks peripheral tolerance

Mast cells (MC) have been shown to mediate regulatory T-cell (T(reg)) dependent, peripheral allograft tolerance in both skin and cardiac transplants. Furthermore, T(reg) have been implicated in mitigating IgE mediated MC degranulation, establishing a dynamic, reciprocal relationship between MC and T(reg) in controlling inflammation. In an allograft tolerance model, it is now shown that intragraft or systemic MC degranulation results in the transient loss of T(reg) suppressor activities with the acute, T-cell dependent rejection of established, tolerant allografts. Upon degranulation, MC mediators can be found in the skin, T(reg) rapidly leave the graft, MC accumulate in the regional lymph node and the T(reg) are impaired in the expression of suppressor molecules. Such a dramatic reversal of T(reg) function and tissue distribution by MC degranulation underscores how allergy may causes the transient breakdown of peripheral tolerance and episodes of acute T-cell inflammation

Mast cells as regulators of adaptive immunity to tumours

The observation that mast cells accumulate at the periphery of growing tumours is now well documented, and the loss of mast cells correlates with reduced tumour growth. The role of mast cells as innate regulators of both inflammatory and immunosuppressive responses slowly becomes clear as novel tools become available. This review will address the role of mast cells in tumours and how they can interact with the local immune environment to mediate immune suppression contributing to tumour escape

Dendritic cells require the NF-kappaB2 pathway for cross-presentation of soluble antigens

NF-kappaB-inducing kinase (NIK) is responsible for activation of the non-canonical p100 processing pathway of NF-kappaB activation. This kinase has been shown to be critical for activation of this pathway after signaling through several TNF family members including CD40. The functional importance of this pathway in CD40 and TLR-induced dendritic cell (DC) differentiation was studied in vivo in the alymphoplasia (Aly) mouse. The Aly mouse expresses a mutant NIK molecule that prohibits the induction of the non-canonical pathway. We show that while MHC class II presentation and in vivo migration of Aly DCs is intact, these cells are unable to cross-prime CD8+ T cells to exogenous Ag. Gene expression array analysis of DCs matured in vivo indicates multiple defects in Ag processing pathways after maturation and provide a global view of the genes that are regulated by the NF-kappaB2 pathway in DCs. These experiments indicate a possible role for NIK in mediating cross-priming of soluble Ag. In addition, our findings explain the profound immune unresponsiveness of the Aly mouse

Tryptophan hydroxylase-1 regulates immune tolerance and inflammation

Nutrient deprivation based on the loss of essential amino acids by catabolic enzymes in the microenvironment is a critical means to control in ammatory responses and immune tolerance. Here we report the novel nding that Tph-1 (tryptophan hydroxylase-1), a synthase which catalyses the conversion of tryptophan to serotonin and exhausts tryptophan, is a potent regulator of immunity. In models of skin allograft tolerance, tumor growth, and experimental autoimmune encephalomyelitis, Tph-1 de ciency breaks allograft tolerance, induces tumor remission, and intensi es neuroin ammation, respectively. All of these effects of Tph-1 de ciency are independent of its downstream product serotonin. Because mast cells (MCs) appear to be the major source of Tph-1 and restoration of Tph-1 in the MC compartment in vivo compensates for the defect, these experiments introduce a fundamentally new mecha- nism of MC-mediated immune suppression that broadly impacts multiple arms of immunity

Cre/loxP-based mouse models of mast cell deficiency and mast cell-specific gene inactivation

Over the past decades, research on in vivo functions of mast cells has largely relied on kit-mutant mouse strains. Recently, new mouse models for investigation of mast cell functions based on the Cre/loxP recombination system have been published and results in these new models challenged findings of previous studies in kit-mutant mice. Herein we describe procedures central to mast cell-specific gene inactivation and the generation of mast cell-deficient mice based on the mouse strain Mcpt5-Cre, which expresses Cre recombinase selectively in connective tissue mast cells