Characterization of monoclonal antibody specific to the Z39Ig protein, a member of immunoglobulin superfamily

Kim, Jin‐Kyung; Choi, Eun Mi; Shin, Hyo-Il; Kim, Chang H.; Hwang, Sunhee; Kim, Seong-Mi; Kwon, Byoung S.

doi:10.1016/j.imlet.2005.02.012

Cited by 21 publications

(18 citation statements)

References 18 publications

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“…We, therefore, examined VSIG4-mediated suppression of LM growth in (nonphagocytic) HeLa cells overexpressing human VSIG4 (HeLa-HsVSIG4). 19 We first determined the optimal MOI of LM in HeLa-mock and HeLa-HsVSIG4 cells. The HeLa cells were infected with the indicated MOI of LM or opLM for 1 h and further incubated for 1 h. When these cells were infected with LM alone for 1 h, their uptake rates were comparable (Fig.…”

Section: Overexpression Of Human Vsig4 On Hela Cells Facilitates Lm Umentioning

confidence: 99%

“…HsVSIG4 stably expressing HeLa cells were generated as as described previously. 19 In brief, full-length VSIG4 was amplified by PCR using the first-strand cDNA of THP-1 cells and a specific primer set (forward including BamHI: 5 0 -CGG GAT CCG AAT TCG GTA CCC GTC CCA TCC TGG AAG TGC CAG AG-3 0 and reverse including NotI: 5 0 -AAG GAA AAA AGC GGC CGC TTA ACA GAC ACT TTT GCC CTC AGT-3 0 ). The PCR products were subcloned into the mammalian expression vector pcDNA3.1 (Invitrogen, V790-20) using BamHI and NotI restriction enzyme sites.…”

Section: Cellsmentioning

confidence: 99%

“…Hybridomas producing monoclonal antibodies to HsVSIG4 and MmVSIG4 were generated by immunizing Balb/c and Sprague Dawley rats with HsVSIG4-and MmVSIG4-transfected HeLa cells, respectively, as described previously. 19 …”

Section: Cellsmentioning

confidence: 99%

“…For in vitro LM killing assays, 19 samples of 2 £ 10 5 cells were plated on 12-well culture plates and incubated with LM (10 MOI) for 1 h at 37 C. The cells were washed with PBS, and exposed to a high concentration of ampicillin (300 mg/ml) for 15 min to remove free LM, and further incubated for 1 h. The infected cells were then treated with 5 mg/ml anti-VSIG4 or control IgG, or serum starved in a 37 C, 5% CO 2 incubator for 0, 2, 4 or 6 h. The cells were lysed in 1 ml of water, and serial dilutions of the lysates were plated on BHI agar.…”

Section: Lm Killing Assaymentioning

confidence: 99%

“…[13][14][15] Autophagy can function as a degradation system detecting microbes that invade the cytosol of the host cell, and can also modulate innate and adaptive immunity, transcriptional signatures for inflammation, and the production and secretion of cytokines including type I IFN. 16,17 VSIG4/CRIg,(V-set and immunoglobulin domain containing 4) is a 50-kDa type I transmembrane receptor that is specifically expressed on monocytes, macrophages, and dendritic cells, 18,19 and is a receptor for the C3b cleavage product of C3 (complement component 3) and inactivated C3b (iC3b). Therefore, complement-opsonized microbes can be efficiently recognized and phagocytosed by VSIG4-expressing macrophages.…”

Section: Introductionmentioning

confidence: 99%

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Extracellular stimulation of VSIG4/complement receptor Ig suppresses intracellular bacterial infection by inducing autophagy

et al. 2016

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VSIG4/CRIg (V-set and immunoglobulin domain containing 4) is a transmembrane receptor of the immunoglobulin superfamily that is expressed specifically on macrophages and mature dendritic cells. VSIG4 signaling accelerates phagocytosis of C3-opsonized bacteria, thereby efficiently clearing pathogens within macrophages. We found that VSIG4 signaling triggered by C3-opsonized Listeria (opLM) or by agonistic anti-VSIG4 monoclonal antibody (mAb) induced macrophages to form autophagosomes. VSIG4-induced autophagosomes were selectively colocalized with the intracellular LM while starvation-induced autophagosomes were not. Consistent with these results, the frequency of autophagosomes induced by infection with opLM was lower in VSIG4-deficient bone marrow-derived macrophages (BMDMs) than in WT BMDMs. Furthermore, when VSIG4 molecules were overexpressed in HeLa cells, which are nonmacrophage cells, VSIG4 triggering led to efficient uptake of LM, autophagosome formation, and killing of the infected LM. These findings suggest that VSIG4 signaling not only promotes rapid phagocytosis and killing of C3-opsonized intracellular bacteria, as previously reported, but also induces autophagosome formation, eliminating the LM that have escaped from phagosomes. We conclude that VSIG4 signaling provides an anti-immune evasion mechanism that prevents the outgrowth of intracellular bacteria in macrophages.

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Section: Overexpression Of Human Vsig4 On Hela Cells Facilitates Lm Umentioning

confidence: 99%

Section: Cellsmentioning

confidence: 99%

Section: Cellsmentioning

confidence: 99%

Section: Lm Killing Assaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Extracellular stimulation of VSIG4/complement receptor Ig suppresses intracellular bacterial infection by inducing autophagy

et al. 2016

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CRIg signals induce anti‐intracellular bacterial phagosome activity in a chloride intracellular channel 3‐dependent manner

et al. 2013

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Macrophages provide a first line of defense against bacterial infection by engulfing and killing invading bacteria, but intracellular bacteria such as Listeria monocytogenes (LM) can survive in macrophages by various mechanisms of evasion. Complement receptor of the immunoglobulin (CRIg), a C3b receptor, binds to C3b on opsonized bacteria and facilitates clearance of the bacteria by promoting their uptake. We found that CRIg signaling induced by agonistic anti-CRIg mAb enhanced the killing of intracellular LM by macrophages, and that this occurred in LM-containing phagosomes. Chloride intracellular channel 3 CLIC3, an intracellular chloride channel protein, was essential for CRIgmediated LM killing by directly interacting with the cytoplasmic domain of CRIg, and the two proteins colocalized on the membranes of LM-containing vacuoles. CLIC3 −/− mice were as susceptible to LM as CRIg −/− mice. These findings identify a mechanism embedded in the process by which macrophages take up opsonized bacteria that prevents the bacteria from evading cell-mediated killing.Keywords: CLIC3 r CRIg r Listeria r Phagosome r Signaling Additional supporting information may be found in the online version of this article at the publisher's web-site

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Costimulatory molecule VSIG4 exclusively expressed on macrophages alleviates renal tubulointerstitial injury in VSIG4 KO mice

Wang

et al. 2014

J Nephrol

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Characterization of monoclonal antibody specific to the Z39Ig protein, a member of immunoglobulin superfamily

Cited by 21 publications

References 18 publications

Extracellular stimulation of VSIG4/complement receptor Ig suppresses intracellular bacterial infection by inducing autophagy

Extracellular stimulation of VSIG4/complement receptor Ig suppresses intracellular bacterial infection by inducing autophagy

CRIg signals induce anti‐intracellular bacterial phagosome activity in a chloride intracellular channel 3‐dependent manner

Costimulatory molecule VSIG4 exclusively expressed on macrophages alleviates renal tubulointerstitial injury in VSIG4 KO mice

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