Modulation of immune response by combined targeting of complement receptors and low-affinity Fcγ receptors

Szekeres, Zsuzsanna; Herbáth, Melinda; Angyal, Adrienn; Szittner, Zoltán; Virág, Viktor; Balogh, Péter; Erdei, Anna; Prechl, József

doi:10.1016/j.imlet.2009.12.002

Cited by 8 publications

(9 citation statements)

References 46 publications

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“…In this study, we examined not only the expression of TrkB within the adrenal gland but also that of the TrkB ligand, BDNF. In contrast to the pattern of TrkB expression, we found BDNF was highly expressed within the rat adrenal cortex, consistent with previous studies (Suter-Crazzolara et al 1996;Schober et al 1999;Szekeres et al 2010). Compared to the cortex, expression of BDNF was significantly lower in the medullary region, where its location was predominantly associated with microvascular cells as previously reported (Wang et al 2006).…”

Section: Paracrine Stimulation Of Chromaffin Cells Via Bdnf-trkb Signsupporting

confidence: 92%

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Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from cultured rat adrenal chromaffin cells

Scott

Zhang

Nurse

2015

The Journal of Physiology

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Key pointsr We investigated the role of the neurotrophin BDNF signalling via the TrkB receptor in rat adrenomedullary chromaffin cells (AMCs) exposed to normoxia (Nox; 21% O 2 ) and chronic hypoxia (CHox; 2% O 2 ) in vitro for ß48 h.r TrkB receptor expression was upregulated in primary AMCs and in immortalized chromaffin (MAH) cells exposed to CHox; this effect was absent in MAH cells deficient in the transcription factor, hypoxia inducible factor (HIF)-2α. Abstract Environmental stressors, including chronic hypoxia, enhance the ability of adrenomedullary chromaffin cells (AMCs) to secrete catecholamines; however, the underlying molecular mechanisms remain unclear. Here, we investigated the role of brain-derived neurotrophic factor (BDNF) signalling in rat AMCs exposed to chronic hypoxia. In rat adrenal glands, BDNF and its tropomyosin-related kinase B (TrkB) receptor are highly expressed in the cortex and medulla, respectively. Exposure of AMCs to chronic hypoxia (2% O 2 ; 48 h) in vitro caused a significant increase to TrkB mRNA expression. A similar increase was observed in an immortalized chromaffin cell line (MAH cells); however, it was absent in MAH cells deficient in the transcription factor HIF-2α. A specific TrkB agonist, 7,

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Section: Paracrine Stimulation Of Chromaffin Cells Via Bdnf-trkb Signsupporting

confidence: 92%

“…; Szekeres et al . ). Compared to the cortex, expression of BDNF was significantly lower in the medullary region, where its location was predominantly associated with microvascular cells as previously reported (Wang et al .…”

Section: Discussionmentioning

confidence: 97%

Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from cultured rat adrenal chromaffin cells

Scott

Zhang

Nurse

2015

The Journal of Physiology

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“…The expanded BM culture was incubated for one additional day without GM-CSF prior to further in vitro tests. Levels of antigen specific IgG1 and IgG2a were determined as described previously [12].…”

Section: Generation Of Bone Marrow-derived Dendritic Cells (Bmdc)mentioning

confidence: 99%

Coadministration of antigen-conjugated and free CpG: Effects of in vitro and in vivo interactions in a murine model

et al. 2014

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“…None of the constructs induced any sign of disease when administered into DBA/1 mice that were not immunized previously with collagen (data not shown). We assumed that the elevation of arthritic scores of collagen primed mice by FcγRII/III targeted CII-peptide and 2.4G2 scFv tetramers might be the result of targeting FcγRII/III positive cells,24,25 including dendritic cells (DC) and macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…Our aim was to investigate how FcγRII/III targeting of this CII peptide by single chain Fv fragment (scFv) of the monoclonal antibody, 2.4G2 may modulate the immunopathogenesis of CIA. Previously we and others have shown that antibody response against model antigens can be substantially improved by FcγRII/III targeting 24,25. Extravidin-linked molecular constructs of the biotinylated CII-peptide and its complex with mono-biotinylated 2.4G2 scFv were injected intravenously into CII pre-immunized DBA/1 mice, and the in vivo effect on several parameters of CIA, including arthritic score, antibody response to CII and CII-peptide, as well as cytokine/chemokine secretion were monitored.…”

Section: Introductionmentioning

confidence: 97%

Exacerbation of collagen induced arthritis by Fcγ receptor targeted collagen peptide due to enhanced inflammatory chemokine and cytokine production

Szarka

Neer

Balogh³

et al. 2012

BTT

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Antibodies specific for bovine type II collagen (CII) and Fcγ receptors play a major role in collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis (RA). Our aim was to clarify the mechanism of immune complex-mediated inflammation and modulation of the disease. CII pre-immunized DBA/1 mice were intravenously boosted with extravidin coupled biotinylated monomeric CII-peptide epitope (ARGLTGRPGDA) and its complexes with biotinylated FcγRII/III specific single chain Fv (scFv) fragment. Disease scores were monitored, antibody titers and cytokines were determined by ELISA, and binding of complexes was detected by flow cytometry and immune histochemistry. Cytokine and chemokine secretion was monitored by protein profiler microarray. When intravenously administered into collagen-primed DBA/1 mice, both CII-peptide and its complex with 2.4G2 scFv significantly accelerated CIA and increased the severity of the disease, whereas the monomeric peptide and monomeric 2.4G2 scFv had no effect. FcγRII/III targeted CII-peptide complexes bound to marginal zone macrophages and dendritic cells, and significantly elevated the synthesis of peptide-specific IgG2a. Furthermore, CII-peptide containing complexes augmented the in vivo secretion of cytokines, including IL-10, IL-12, IL-17, IL-23, and chemokines (CXCL13, MIP-1, MIP-2). These data indicate that complexes formed by the CII-peptide epitope aggravate CIA by inducing the secretion of chemokines and the IL-12/23 family of pro-inflammatory cytokines. Taken together, these results suggest that the in vivo emerging immune complexes formed with autoantigen(s) may trigger the IL-12/23 dependent pathways, escalating the inflammation in RA. Thus blockade of these cytokines may be beneficial to downregulate immune complex-induced inflammation in autoimmune arthritis.

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Modulation of immune response by combined targeting of complement receptors and low-affinity Fcγ receptors

Cited by 8 publications

References 46 publications

Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from cultured rat adrenal chromaffin cells

Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from cultured rat adrenal chromaffin cells

Coadministration of antigen-conjugated and free CpG: Effects of in vitro and in vivo interactions in a murine model

Exacerbation of collagen induced arthritis by Fcγ receptor targeted collagen peptide due to enhanced inflammatory chemokine and cytokine production

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Modulation of immune response by combined targeting of complement receptors and low-affinity Fcγ receptors

Cited by 8 publications

References 46 publications

Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from cultured rat adrenal chromaffin cells

Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from cultured rat adrenal chromaffin cells

Coadministration of antigen-conjugated and free CpG: Effects of in vitro and in vivo interactions in a murine model

Exacerbation of collagen induced arthritis by Fc&gamma; receptor targeted collagen peptide due to enhanced inflammatory chemokine and cytokine production

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Exacerbation of collagen induced arthritis by Fcγ receptor targeted collagen peptide due to enhanced inflammatory chemokine and cytokine production