Scavenger receptor class B type I: a multifunctional receptor

Valacchi, Giuseppe; Sticozzi, Claudia; Lim, Yunsook; Pecorelli, Alessandra

doi:10.1111/j.1749-6632.2011.06205.x

Cited by 93 publications

(76 citation statements)

References 80 publications

(178 reference statements)

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“…3a), (ii) in bone marrow, muscle, testis, thymus, spinal cord, and brain, the concentration, albeit quite low overall, rises steadily with time suggesting a very delayed distribution. The first group of organs has higher expression of SR-B1, [22][23][24] and the data match the plasma circulation indeed, suggesting a fast diffusion from the blood to the tissues. In the other organs, particularly the poorly perfused, the steady rise in polymersome concentration could be explained by monocyte/macrophage penetration into tissues over time.…”

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confidence: 55%

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Targeting mononuclear phagocytes for eradicating intracellular parasites

Rizzello

Robertson

Elks

et al. 2017

Preprint

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Mononuclear phagocytes such as monocytes, tissue-specific macrophages and dendritic cells are primary actors in both innate and adaptive immunity, as well as tissue homoeostasis. They have key roles in a range of physiological and pathological processes, so any strategy targeting these cells will have wide-ranging impact. These phagocytes can be parasitized by intracellular bacteria, turning them from housekeepers to hiding places and favouring chronic and/or disseminated infection. One of the most infamous is the bacteria that cause tuberculosis, which is the most pandemic and one of the deadliest disease with one third of the world's population infected, and 1.8 million deaths worldwide in 2015. Here we demonstrate the effective targeting and intracellular delivery of antibiotics to both circulating monocytes and resident macrophages, using pH sensitive nanoscopic polymersomes made of poly(2-(methacryloyloxy)ethyl phosphorylcholine)-co-poly(2-(diisopropylamino)ethyl methacrylate) (PMPC-PDPA). Polymersome selectivity to mononuclear phagocytes is demonstrated and ascribed to the polymerised phosphorylcholine motifs affinity toward scavenger receptors. Finally, we demonstrate the successful exploitation of this targeting for the effective eradication of intracellular bacteria that cause tuberculosis Mycobacterium tuberculosis as well as other intracellular parasites including the Mycobacterium bovis, Mycobacterium marinum and the most common bacteria associated with antibiotic resistance, the Staphylococcus aureus.

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confidence: 55%

“…[22][23][24] To test whether macrophages also internalise polymersomes using scavenger receptors, we incubated the cells with fucoidan, an inhibitor of Scavenger Receptors class A and B (SR-A and B). Despite the presence of the inhibitor, polymersomes were able to access macrophages, albeit with a considerable decrease in uptake of about 40% (Figure 2b).…”

mentioning

confidence: 99%

Targeting mononuclear phagocytes for eradicating intracellular parasites

Rizzello

Robertson

Elks

et al. 2017

Preprint

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“…The wide expression in a range of different tissues is due to the essential role of SR-B1 in lipid metabolism. SR-B1 is a well-characterized lipoprotein receptor that binds native lipoproteins such as high, and low-density lipoproteins (HDL and LDL, respectively) [71]. There is an alternative splicing variant of SR-B1 (SR-B1.2) differing in C-terminal amino acid sequence, tissue expression pattern and ligand-binding specificity [72].…”

Section: Sr-b1 (Scavenger Receptor Class B Type 1)mentioning

confidence: 99%

Exploiting scavenger receptors in cancer immunotherapy: Lessons from CD5 and SR‐B1

et al. 2017

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Scavenger receptors (SRs) are structurally heterogeneous cell surface receptors characterized by their capacity to remove extraneous or modified self-macromolecules from circulation, thus avoiding the accumulation of noxious agents in the extracellular space. This scavenging activity makes SRs important molecules for host defense and homeostasis. In turn, SRs keep the activation of the steady-state immune response in check, and participate as co-receptors in the priming of the effector immune responses when the macromolecules are associated with a threat that might compromise host homeostasis. Therefore, SRs built up sophisticated sensor mechanisms controlling the immune system, which may be exploited to develop novel drugs for cancer immunotherapy. In this review, we focus on the regulation of the anti-tumor immune response by two paradigmatic SRs: the lymphocyte receptor CD5 and the more broadly distributed scavenger receptor class B type 1 (SR-B1). Cancer immunity can be boosted by blockade of SRs working as immune checkpoint inhibitors (CD5) and/or by proper engagement of SRs working as innate danger receptor (SR-B1). Thus, these receptors illustrate both the complexity of targeting SRs in cancer immunotherapy and also the opportunities offered by such an approach. Keywords:Cancer immunotherapy r CD5 r Danger signal r Immune-checkpoint r Scavenger receptor r Scavenger receptor class B type 1 r Toll-like receptors IntroductionThe cancer-immunity cycle can be subverted by tumors at many steps, thus novel therapeutic interventions should be considered for all these possibilities [1]. This cycle starts with the release of tumor antigens and their subsequent capture by professional antigen-presenting cells (mainly, dendritic cells; DCs) for the activation of effector cells of the innate and adaptive immune Correspondence: Dr. Pedro Berraondo e-mail: pberraondol@unav.es system. This is a highly regulated process aimed at maintaining the integrity of the host without inducing significant side effects (e.g., inflammation or autoimmunity) [2]. Tissue homeostasis involves phagocytic processes to remove the excess of native or modified molecules from unviable or stressed cells, as well as from invading microbial agents [3]. Such molecules include lipids, whose intracellular levels should be carefully controlled to sustain proper cell metabolism; endogenous glyco-and lipo-proteins, damaged or * These authors contributed equally to this work. * * These authors are senior co-authors of this work. [4,5]. This phagocytic activity should be coupled to an alarm signal system that awakens other effector mechanisms of the immune system when the tissue damage cannot be controlled by the removal of the endogenous or exogenous molecules. To this end, the immune system has a myriad of specialized soluble or membrane-bound receptors called pattern recognition receptors (PRRs). These PRRs are non-polymorphic, nonclonally distributed, and germ-line encoded receptors recognizing microorganism-associated molecular patterns (MAMPs) -tha...

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“…However, LRPs have now been shown to interact with 30 different ligands and perform diverse roles such as uptake of lipoproteins, glucose regulation, transport of ligands across the blood-brain barrier, and Wnt/β-catenin signaling (51)(52)(53)(54). Similarly, the cell surface HDL receptor SR-BI is involved in cholesterol uptake, vitamin E transport, host defense, and removal of apoptotic cells (55,56). It is therefore plausible that ILDR1 performs distinct functions in different tissues.…”

Section: Figurementioning

confidence: 99%

Immunoglobulin-like domain containing receptor 1 mediates fat-stimulated cholecystokinin secretion

Chandra

Wang²,

Shahid³

et al. 2013

J. Clin. Invest.

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Cholecystokinin (CCK) is a satiety hormone produced by discrete enteroendocrine cells scattered among absorptive cells of the small intestine. CCK is released into blood following a meal; however, the mechanisms inducing hormone secretion are largely unknown. Ingested fat is the major stimulant of CCK secretion. We recently identified a novel member of the lipoprotein remnant receptor family known as immunoglobulinlike domain containing receptor 1 (ILDR1) in intestinal CCK cells and postulated that this receptor conveyed the signal for fat-stimulated CCK secretion. In the intestine, ILDR1 is expressed exclusively in CCK cells. Orogastric administration of fatty acids elevated blood levels of CCK in wild-type mice but not Ildr1-deficient mice, although the CCK secretory response to trypsin inhibitor was retained. The uptake of fluorescently labeled lipoproteins in ILDR1-transfected CHO cells and release of CCK from isolated intestinal cells required a unique combination of fatty acid plus HDL. CCK secretion secondary to ILDR1 activation was associated with increased [Ca 2+ ] i , consistent with regulated hormone release. These findings demonstrate that ILDR1 regulates CCK release through a mechanism dependent on fatty acids and lipoproteins and that absorbed fatty acids regulate gastrointestinal hormone secretion.

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Scavenger receptor class B type I: a multifunctional receptor

Cited by 93 publications

References 80 publications

Targeting mononuclear phagocytes for eradicating intracellular parasites

Targeting mononuclear phagocytes for eradicating intracellular parasites

Exploiting scavenger receptors in cancer immunotherapy: Lessons from CD5 and SR‐B1

Immunoglobulin-like domain containing receptor 1 mediates fat-stimulated cholecystokinin secretion

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