To be or not to be B7

Zang, Xingxing; Allison, James P.

doi:10.1172/jci30103

Cited by 23 publications

(21 citation statements)

References 16 publications

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“…However, these are not liver KC-specific. Here, we evaluate the imaging capacity of two recently recognized KC markers, namely Clec4F and Vsig4 [13,14,16]. monocytes).…”

Section: Discussionmentioning

confidence: 99%

“…Clec4F is exclusively expressed on KCs in mice, but is not applicable in humans where Clec4F orthologue expression can be found in other tissues, mainly the colon, the brain, the testis or ovary [33]. Despite reports showing that Vsig4 is expressed transiently on distinct subsets of resident macrophages throughout the body [14], this did not appear to limit the effectiveness of using Vsig4 Nbs to non-invasively image KCs neither in the models investigated herein nor in our previous results [13]. In addition, our results obtained with Vsig4 Nbs are congruent with those obtained with the exclusive KC marker Clec4F.…”

Section: Discussionmentioning

confidence: 99%

“…In this context, we have recently demonstrated that Nbs targeting Vsig4 can be used as a method to non-invasively image KC dynamics via singlephoton emission computed tomography/micro X-ray computed tomography (SPECT/μCT) during the progression and resolution of ConA-induced auto-immune hepatitis [13]. However, Vsig4 is not strictly a KC marker but is rather mainly expressed on a subset of resident macrophages in the liver, heart, adrenal glands, lungs, and peritoneal cavity, in particular, during inflammatory conditions [14]. Haltiwagner, et al [15] demonstrated that Clec4F is expressed by resident macrophages in the murine liver.…”

Section: Introductionmentioning

confidence: 99%

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Molecular Imaging with Kupffer Cell-Targeting Nanobodies for Diagnosis and Prognosis in Mouse Models of Liver Pathogenesis

et al. 2016

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“…However, these are not liver KC-specific. Here, we evaluate the imaging capacity of two recently recognized KC markers, namely Clec4F and Vsig4 [13,14,16]. monocytes).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Molecular Imaging with Kupffer Cell-Targeting Nanobodies for Diagnosis and Prognosis in Mouse Models of Liver Pathogenesis

et al. 2016

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“…They described the complement-binding properties of CRIg and developed a CRIg-Fc fusion protein capable of inhibiting alternative complement pathway activation (6)(7)(8) and providing protection against experimental arthritis (9). The immunosuppressive action of CRIg on T cells has also been highlighted (10,11). Others have reported its anti-inflammatory properties in experimental autoimmune uveoretinitis (12), intestinal ischemia/reperfusion-induced injury (9), and immune-mediated liver injury (13).…”

mentioning

confidence: 99%

Protein Kinase Cα Regulates the Expression of Complement Receptor Ig in Human Monocyte–Derived Macrophages

Usuwanthim

Munawara

et al. 2015

The Journal of Immunology

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The complement receptor Ig (CRIg) is selectively expressed by macrophages. This receptor not only promotes the rapid phagocytosis of bacteria by macrophages but also has anti-inflammatory and immunosuppressive functions. Previous findings have suggested that protein kinase C (PKC) may be involved in the regulation of CRIg expression in human macrophages. We have now examined the role of PKCα in CRIg expression in human monocyte-derived macrophages (MDM). Macrophages nucleofected with plasmid containing short hairpin RNA against PKCα showed markedly reduced expression of PKCα, but normal PKCζ expression, by Western blotting analysis, and vice versa. PKCα-deficient MDM showed increased expression of CRIg mRNA and protein (both the long and short form), an increase in phagocytosis of complement-opsonized Candida albicans, and decreased production of TNF-α and IL-6. TNF-α caused a marked decrease in CRIg expression, and addition of anti-TNF mAb to the TNF-α–producing MDMs increased CRIg expression. PKCα-deficient macrophages also showed significantly less bacterial LPS-induced downregulation of CRIg. In contrast, cells deficient in PKCα showed decreased expression of CR type 3 (CR3) and decreased production of TNF-α and IL-6 in response to LPS. MDM developed under conditions that increased expression of CRIg over CR3 showed significantly reduced production of TNF-α in response to opsonized C. albicans. The findings indicate that PKCα promotes the downregulation of CRIg and upregulation of CR3 expression and TNF-α and IL-6 production, a mechanism that may promote inflammation.

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“…Complement receptor immunoglobulin (CRIg), a recently discovered complement receptor, enhances complement-mediated phagocytosis of macrophages and can negatively regulate T cell activation. 1 CRIg is transmembrane protein type 1 immunoglobulin superfamily which encoded by VISIG gene located in X chromosome. 2 CRIg play critical role in both innate and adaptive immune system.…”

Section: Introductionmentioning

confidence: 99%

Expression of Complement Receptor Immunoglobulin in Human Monocyte-Derived Macrophages

Kooltheat¹,

Wisitpongpun²,

Potup³

et al. 2017

Int. J. Res. Ayurveda Pharm.

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The complement receptor of the immunoglobulin (CRIg) is exclusively express by macrophages. This complement receptor play critical role not only in innate immunity but also adaptive immune response. Previous study has suggested that PKC involved in the regulation of CRIg expression in human macrophages. In this study, we have examined the role of glucocorticoid receptor in CRIg expression in human monocyte-derived macrophages (MDMs). Human macrophages nucleofected with plasmid containing short hairpin RNA against glucocorticoid receptor showed reduced expression of glucocorticoid receptor mRNA and protein by RT-qPCR and Western blot analysis, respectively. Glucocorticoid receptordeficient MDMs showed decreased expression of CRIg mRNA and protein (long and short form). In contrast, cell deficient in glucocorticoid receptor showed increased expression of CRIg in response to dexamethasone. The finding indicates that glucocorticoid receptor involves in the regulation of CRIg expression and dexamethasone promotes the up-regulation of CRIg expression via glucocorticoid receptor.

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To be or not to be B7

Cited by 23 publications

References 16 publications

Molecular Imaging with Kupffer Cell-Targeting Nanobodies for Diagnosis and Prognosis in Mouse Models of Liver Pathogenesis

Molecular Imaging with Kupffer Cell-Targeting Nanobodies for Diagnosis and Prognosis in Mouse Models of Liver Pathogenesis

Protein Kinase Cα Regulates the Expression of Complement Receptor Ig in Human Monocyte–Derived Macrophages

Expression of Complement Receptor Immunoglobulin in Human Monocyte-Derived Macrophages

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