Anaphylaxis and Mortality Induced by Treatment of Mice with Anti–VLA-4 Antibody and Pertussis Toxin

Ji, Niannian; Rao, Nagarjun; Guentzel, Neal; Arulanandam, Bernard P.; Forsthuber, Thomas G.

doi:10.4049/jimmunol.1000907

Cited by 5 publications

(5 citation statements)

References 46 publications

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“…Mice for EAE induction without PTX need a fivefold dosage of self‐peptide to induce anaphylaxis as compared to EAE mice treated with PTX . Anti‐very late appearing antigen‐4 antibody induced anaphylaxis is correlated with high levels of mortality in PTX‐injected EAE mice, but not in PTX‐untreated mice . Here, we show that PTX can increase the vascular permeability, which is consistent with previous findings that lack sphingosine‐1‐phosphate in plasma or PI3K‐C2α knockdown in endothelial cells or treatment with IL‐4/IL‐13 or IL‐33 exhibit higher vascular permeability that result in susceptibility to anaphylaxis .…”

Section: Discussionsupporting

confidence: 90%

Basophil activation through ASGM1 stimulation triggers PAF release and anaphylaxis‐like shock in mice

Yang

Katirai

et al. 2014

Eur J Immunol

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Basophils have been shown to contribute to anaphylaxis through either an IgE-FcεRI-dependent pathway or an IgG-FcγR pathway. However, it remains largely unclear whether basophils can be activated to promote anaphylaxis via a non-FcR pathway as well. The glycolipid receptor ASGM1 (Asialoganglioside gangliotetraosylceramide), which has an exposed GalNAcβ1-4Gal moiety and serves as a receptor for pathogen associated molecular patterns such as flagellin, was recently found to be expressed on basophils. Here, we demonstrate that stimulation of basophils with anti-ASGM1 antibodies promotes platelet-activating factor (PAF) secretion in vitro and in vivo. Moreover, we found that ASGM1 stimulation triggers basophil-and PAF-dependent anaphylactic shock in pertussis toxin (PTX)-pretreated mice. Thus, ASGM1 has a crucial role in basophil activation and basophil-mediated anaphylaxis-like shock in mice, especially when the vascular permeability is increased by PTX treatment. Our findings describe a novel anaphylaxisassociated pathway that is antigen-, antibody-, and FcR-independent.Keywords: Anaphylaxis r ASGM1 r Basophil r PAF Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionAnaphylaxis is a serious life-threatening allergic reaction characterized by rapid onset and potentially fatal outcomes [1]. The major manifestations of anaphylaxis include bronchoconstriction, pulmonary hypertension, systemic hypotension, and vascular leakage. A classical IgE-and FcεRI-dependent pathway has long been recognized to be associated with anaphylaxis. Binding of Correspondence: Dr. Fang Zheng e-mail: zhengfangtj@hust.edu.cn antigens to IgE and high-affinity cross-linking with FcεRI trigger the release of histamines from mast cells, resulting in anaphylaxis. Recently, various human and animal studies have indicated that IgG-and FcγR-involving pathways also mediate anaphylaxis in an IgE-independent fashion [2][3][4]. IgG antibodies, FcγRIIIA and FcγRIV, macrophages and neutrophils, as well as plateletactivating factor (PAF) are the main players in IgG-induced passive and active systemic anaphylaxis, in which IgE antibodies, FcεRI, mast cells, and histamine play a minor role [5]. It has been reported that in the absence of a specific allergen and antibodies, treatment with two injections of the cytokine IL-33 can trigger a third pathway for anaphylaxis in mice [6]. Kojimawww.eji-journal.eu Eur. J. Immunol. 2014. 44: 2468-2477 Innate immunity 2469 et al. also reported that in mice the anti-CD200R3 antibody Ba91 induced systemic and local anaphylaxis via an IgE-and IgG1-independent pathway that involved CD200R3 receptor activation [7]. Currently, it is largely unclear whether and how non-FcR receptors activate immune cells and trigger anaphylaxis. Basophils represent less than 1% of peripheral blood leukocytes. They are thought to contribute to anaphylaxis by releasing histamine and PAF. It has long been recognized that antigen binding to IgE and high-affinity cross-linkin...

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Section: Discussionsupporting

confidence: 90%

Basophil activation through ASGM1 stimulation triggers PAF release and anaphylaxis‐like shock in mice

Yang

Katirai

et al. 2014

Eur J Immunol

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“…To address this issue, EAE was induced in C57BL/6 mice with MOG 35-55 peptide or via adoptive transfer of PLP 139-151 -reactive T cells in SJL mice as previously described (30). CNS tissue was obtained at the peak of disease and analyzed by confocal microscopy for colocalization of MBP, MOG, or PLP with myeloid cells.…”

Section: Resultsmentioning

confidence: 99%

“…To address this question, EAE was induced in C57BL/6 mice with MOG 35-55 peptide as described (30). Representative animals were sacrificed daily starting one day after immunization and CNS tissue sections were obtained for confocal microscopy analysis and quantification of CD4 + T cells and various APC populations present.…”

Section: Resultsmentioning

confidence: 99%

The Kinetics of Myelin Antigen Uptake by Myeloid Cells in the Central Nervous System during Experimental Autoimmune Encephalomyelitis

Sosa

Murphey

et al. 2013

The Journal of Immunology

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Induction of experimental autoimmune encephalomyelitis (EAE) in susceptible animals requires reactivation of encephalitogenic CD4+ T cells by antigen presenting cells (APCs) in the central nervous system (CNS). However, it has remained unresolved from where APCs in the CNS acquire myelin antigen (Ag) for T cell activation and under which conditions, i.e. whether only during EAE or also in the naïve CNS. Here, we investigated the kinetics of myelin Ag uptake by CNS APCs during EAE and in the naïve CNS. Our results show that during EAE CX3CR1+CD11b+ microglia were the first APCs in the CNS to contain myelin Ag upon induction of disease, albeit in very small numbers. Dendritic cells (DCs) arrived in the CNS in sizable numbers significantly later (day 5 post-immunization (p.i.)), without detectable myelin Ag, but acquired it by day 7 p.i. Furthermore, a sharp increase in neuroantigen-containing DCs coincided with the onset of EAE symptoms. Importantly, in naïve mice a low but consistent number of microglia contained myelin Ag, suggesting release by oligodendrocytes under steady state conditions. Although microglia isolated from naïve brain and spinal cord did not elicit a strong CD4+ T cell response in vitro, myelin Ag-containing microglia may still play a local role in modulating encephalitogenic CD4+ T cell responses in early EAE prior to the arrival of other professional APCs such as DCs. Finally, newly arriving DCs in the CNS not yet loaded with myelin Ag before the onset of EAE may be a potential therapeutic target.

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“…Under physiologic flow rates in the hepatic sinusoids (Shetty et al, 2014), the number of rolling and adhesion cells to LSECs was markedly increased in HFD-fed mice compared with SD-fed mice (Figure 4E). When WEHI 274.1 cells were pretreated with blocking antibodies against integrins (LFA-1, VLA-4, or PSGL-1) (Balasa et al, 2015;Ji et al, 2011; (legend continued on next page) Wang et al, 2012), monocyte adhesion to LSECs of HFD-fed mice was inhibited by anti-VLA-4 blocking antibody (Figure 4F). On transendothelial migration assays under static condition, VLA-4 blockade of WEHI 274.1 cells reduced cell transmigration across LSECs of HFD-fed mice (Figure 4G).…”

Section: Obesity Enhances Myeloid Cell Adhesion and Transmigration Across Lsecs Via Vla-4-dependent Mannermentioning

confidence: 99%

Roles for Cell-Cell Adhesion and Contact in Obesity-Induced Hepatic Myeloid Cell Accumulation and Glucose Intolerance

et al. 2017

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Obesity promotes infiltration of inflammatory cells into various tissues, leading to parenchymal and stromal cell interaction and development of cellular and organ dysfunction. Liver sinusoidal endothelial cells (LSECs) are the first cells that contact portal blood cells and substances in the liver, but their functions in the development of obesity-associated glucose metabolism remain unclear. Here, we find that LSECs are involved in obesity-associated accumulation of myeloid cells via VLA-4-dependent cell-cell adhesion. VLA-4 blockade in mice fed a high-fat diet attenuated myeloid cell accumulation in the liver to improve hepatic inflammation and systemic glucose intolerance. Ex vivo studies further show that cell-cell contact between intrahepatic leukocytes and parenchymal hepatocytes induces gluconeogenesis via a Notch-dependent pathway. These findings suggest that cell-cell interaction between parenchymal and stromal cells regulates hepatic glucose metabolism and offers potential strategies for treatment or prevention of obesity-associated glucose intolerance.

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Anaphylaxis and Mortality Induced by Treatment of Mice with Anti–VLA-4 Antibody and Pertussis Toxin

Cited by 5 publications

References 46 publications

Basophil activation through ASGM1 stimulation triggers PAF release and anaphylaxis‐like shock in mice

Basophil activation through ASGM1 stimulation triggers PAF release and anaphylaxis‐like shock in mice

The Kinetics of Myelin Antigen Uptake by Myeloid Cells in the Central Nervous System during Experimental Autoimmune Encephalomyelitis

Roles for Cell-Cell Adhesion and Contact in Obesity-Induced Hepatic Myeloid Cell Accumulation and Glucose Intolerance

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