Myosin II synergizes with F-actin to promote DNGR-1-dependent cross-presentation of dead cell-associated antigens

Conventional type 1 DCs (cDC1s) excel at cross-presentation of dead cell-associated antigens partly because they express DNGR-1, a receptor that recognizes exposed actin filaments on dead cells. In vitro polymerized F-actin can be used as a synthetic ligand for DNGR-1. However, cellular F-actin is decorated with actin-binding proteins, which could affect DNGR-1 recognition. Here, we demonstrate that myosin II, an F-actin-associated motor protein, greatly potentiates the binding of DNGR-1 to F-actin. Latex beads coated with F-actin and myosin II are taken up by DNGR-1+ cDC1s, and antigen associated with those beads is efficiently cross-presented to CD8+ T cells. Myosin II-deficient necrotic cells are impaired in their ability to stimulate DNGR-1 or to serve as substrates for cDC1 cross-presentation to CD8+ T cells. These results provide insights into the nature of the DNGR-1 ligand and have implications for understanding immune responses to cell-associated antigens and for vaccine design

Zachowanie Cd, Cr, Cu, Pb i Zn w glebach napływowej i brunatnej nawożonych kompostami

Risk elements contents play important role in compost quality determination. The aim of the work was to evaluate main risk elements availability in two soils with various parameters after composts application. The changes of risk elements mobility in soils fertilized with composts differed in dependence on soil parameters (risk elements contamination of soil, clay particles content, organic matter content and pH value) and on used extraction agent. Cadmium, zinc and partly chromium extracted in 0.01 mol o dm^-3 CaCl2 solution were immobilized and lead was released to soil solution of both soils. The remediation ability of composts in cadmium and lead contaminated soil was found only for cadmium.Zawartość pierwiastków szkodliwych odgrywa ważną rolę w wyznaczaniu jakości kompostu. Celem badań była ocena przyswajalności głównych pierwiastków szkodliwych w dwóch glebach o różnych parametrach po zastosowaniu kompostów. Zmiany mobilności tych pierwiastków w glebach nawożonych kompostami różniły się w zależności od właściwości gleby (zanieczyszczenia gleb pierwiastkami szkodliwymi, zawartości frakcji iłu, zawartości materii organicznej i wartości pH) i od użytego odczynnika ekstrakcyjnego. Kadm, cynk i częściowo chrom ekstrahowane roztworem 0,01 mol CaCl2 o dm^-3 były unieruchamiane, a ołów był uwalniany do roztworu glebowego obydwu gleb. Zdolność remediacyjną kompostu w glebach zanieczyszczonych kadmem i ołowiem stwierdzono tylko w przypadku kadmu

Sensing Tissue Damage by Myeloid C-Type Lectin Receptors

After both sterile and infectious insults, damage is inflicted on tissues leading to accidental or programmed cell death. In addition, events of programmed cell death also take place under homeostatic conditions, such as in embryo development or in the turnover of hematopoietic cells. Mammalian tissues are seeded with myeloid immune cells, which harbor a plethora of receptors that allow the detection of cell death, modulating immune responses. The myeloid C-type lectin receptors (CLRs) are one of the most prominent families of receptors involved in tailoring immunity after sensing dead cells. In this chapter, we will cover a diversity of signals arising from different forms of cell death and how they are recognized by myeloid CLRs. We will also explore how myeloid cells develop their sentinel function, exploring how some of these CLRs identify cell death and the type of responses triggered thereof. In particular, we will focus on DNGR-1 (CLEC9A), Mincle (CLEC4E), CLL-1 (CLEC12A), LOX-1 (OLR1), CD301 (CLEC10A) and DEC-205 (LY75) as paradigmatic death-sensing CLRs expressed by myeloid cells. The molecular processes triggered after cell death recognition by myeloid CLRs contribute to the regulation of immune responses in pathologies associated with tissue damage, such as infection, autoimmunity and cancer. A better understanding of these processes may help to improve the current approaches for therapeutic intervention.Carlos Del Fresno is supported by AECC Foundation (INVES192DELF). Francisco Javier Cueto is the recipient of a Ph.D. “La Caixa” fellowship (LCF/BQ/ES14/10320011). Work in the DS laboratory is funded by the CNIC; by the European Research Council (ERC-2016-Consolidator Grant 725091); by the European Commission (635122-PROCROP H2020); by Ministerio de Ciencia, Innovación e Universidades (MICINN), Agencia Estatal de Investigación and Fondo Europeo de Desarrollo Regional (FEDER) (SAF2016-79040-R); by Comunidad de Madrid (B2017/BMD-3733 Immunothercan-CM); by FIS-Instituto de Salud Carlos III, MICINN and FEDER (RD16/0015/0018-REEM); by Acteria Foundation; by Atresmedia (Constantes y Vitales prize) and by Fundació La Marató de TV3 (201723). The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the MICINN and the Pro-CNIC Foundation and is a Severo Ochoa Center of Excellence (SEV-2015-0505).S