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van der Vlist, M.

Publications and source records attributed to van der Vlist, M..

4 recordsLinked to original sources

A novel bioinformatics pipeline for the identification of immune inhibitory receptors as potential therapeutic targets

Blocking inhibitory receptors like PD-1 and CTLA-4 has revolutionized cancer treatment in recent years. However, despite major successes in melanoma and lung cancer, the majority of cancer types are not responsive to these immunotherapies. As such, there is an ongoing need for the identification of novel inhibitory receptors as drug targets. Most inhibitory receptors signal via immunoreceptor tyrosine-based inhibitory motifs (ITIMs) and previous studies have estimated that our genome contains over 1600 ITIM- bearing transmembrane proteins. However, further testing and development of this large number of candidates requires increased understanding of their expression patterns and likelihood to function as inhibitory receptor. To assist in the selection of novel inhibitory receptor as therapeutic targets, we designed a novel bioinformatics pipeline integrating machine learning-guided structural predictions and sequence-based likelihood models to identify 51 known and 390 putative inhibitory receptors. Using publicly available transcriptomics data of immune cells, we determined the expression of these novel inhibitory receptors, and classified them into previously proposed functional categories. Known and putative inhibitory receptors were expressed across a wide variety of immune cells, and we found cell type-specific patterns in expression of these receptors. We used our pipeline to study inhibitory receptor expression patterns in single cell transcriptomics data of tumour infiltrating T cells. We determined that putative immune inhibitory receptors were expressed differentially in CD4+ and CD8+ T cell subsets, including exhausted CD8+ T cells and CD4+ memory T cells, which could allow for subset-specific targeting. In conclusion, we present an inhibitory receptor pipeline that identifies 51 known and 390 novel inhibitory receptors. This pipeline will support future drug target selection across diseases where therapeutic targeting of immune inhibitory receptors is warranted.

immunology↗

Identification of a novel conserved signaling motif in CD200 Receptor required for its inhibitory function

The inhibitory signaling of CD200 receptor 1 (CD200R) has been attributed to its NPxY signaling motif. However, NPxY-motifs are present in multiple protein families and are mostly known to mediate protein trafficking between subcellular locations rather than signaling. Therefore, we investigated whether additional motifs specify the inhibitory function of CD200R. We performed phylogenetic analysis of the intracellular domain of CD200R in mammals, birds, bony fish, amphibians and reptiles. Indeed, the tyrosine of the NPxY-motif is fully conserved across species, in line with its central role in CD200R signaling. In contrast, P295 of the NPxY-motif is not conserved. Instead, a conserved stretch of negatively charged amino acids, EEDE279, and two conserved residues P285 and K292 in the flanking region prior to the NPxY-motif are required for CD200R mediated inhibition of p-Erk, p-Akt308, p-Akt473, p-rpS6 and LPS-induced IL-8 secretion. Altogether, we show that instead of the more common NPxY-motif, CD200R signaling can be assigned to a unique signaling motif in mammals defined by: EEDExxPYxxYxxKxNxxY.

immunology↗

Inhibitory CD200-receptor signaling is rewired by type I interferon

CD200 Receptor 1 (CD200R) is an established inhibitory immune receptor that inhibits TLR-induced cytokine production through Dok2 and RasGAP. RasGAP can be cleaved under certain conditions of mild cellular stress. We found that in the presence of cleaved RasGAP, CD200R loses its capacity to inhibit rpS6 phosphorylation. Furthermore, IFN pre-stimulation of human mononuclear cells results in increased amounts of cleaved RasGAP. Coherently, upon pretreatment with increasing concentrations of IFN, CD200R gradually shifts from an inhibitor to a potentiator of TLR7/8-induced IFNG mRNA production. In peripheral blood mononuclear cells from Systemic Lupus Erythematosus (SLE) patients, a prototypic type I IFN disease, we found an increased proportion of cleaved RasGAP compared to healthy controls. In line with this, in subsets of SLE patients the inhibitory function of CD200R is lost or converted to a potentiating signal for IFNG mRNA production. Thus, our data show that type I IFN rewires CD200R signaling and suggest that this cell-extrinsic regulation of signaling could contribute to perpetuation of inflammation in SLE.

immunology↗

Macrophages transfer mitochondria to neurons to resolve inflammatory pain

The current paradigm is that inflammatory pain passively resolves following the cessation of inflammation. Yet, in a substantial proportion of patients with inflammatory diseases, resolution of inflammation is not sufficient to resolve pain, resulting in chronic pain. Mechanistic insight how inflammatory pain is resolved is lacking. Here we show that macrophages actively control resolution of inflammatory pain remotely from the site of inflammation by transferring mitochondria to sensory neurons. During resolution of inflammatory pain in mice, M2-like macrophages infiltrate the dorsal root ganglia that contain the somata of sensory neurons, concurrent with the recovery of oxidative phosphorylation in sensory neurons. The resolution of pain and the transfer of mitochondria requires expression of CD200 Receptor (CD200R) on macrophages and the non-canonical CD200R-ligand iSec1 on sensory neurons. Our data reveal a novel mechanism for active resolution of inflammatory pain. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=172 SRC="FIGDIR/small/940445v3_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@1048f6org.highwire.dtl.DTLVardef@1262306org.highwire.dtl.DTLVardef@c58261org.highwire.dtl.DTLVardef@f2d4a0_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗