Effects of anti-IgE mAb on serum IgE, FcεRII/CD23 expression on splenic B cells and worm burden in mice infected with Paragonimus westermani

Shin, Myoung-Ho; Hou, Min

doi:10.3347/kjp.1997.35.1.47

Cited by 8 publications

(3 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Under some conditions, however, systemic IgE may reach pathogenic levels. Parasitic infection (e.g., Paragonimus westermani) enhances mouse serum IgE levels to approximately 50 μg/ml (44). Patients with the hyperimmunoglobulin E recurrent infection syndrome (HIES) have serum IgE levels of approximately 72-86 μg/ml (45).…”

Section: Figurementioning

confidence: 99%

IgE stimulates human and mouse arterial cell apoptosis and cytokine expression and promotes atherogenesis in Apoe–/– mice

et al. 2011

View full text Add to dashboard Cite

IgE has a key role in the pathogenesis of allergic responses through its ability to activate mast cells via the receptor FcεR1. In addition to mast cells, many cell types implicated in atherogenesis express FcεR1, but whether IgE has a role in this disease has not been determined. Here, we demonstrate that serum IgE levels are elevated in patients with myocardial infarction or unstable angina pectoris. We found that IgE and the FcεR1 subunit FcεR1α were present in human atherosclerotic lesions and that they localized particularly to macrophagerich areas. In mice, absence of FcεR1α reduced inflammation and apoptosis in atherosclerotic plaques and reduced the burden of disease. In cultured macrophages, the presence of TLR4 was required for FcεR1 activity. IgE stimulated the interaction between FcεR1 and TLR4, thereby inducing macrophage signal transduction, inflammatory molecule expression, and apoptosis. These IgE activities were reduced in the absence of FcεR1 or TLR4. Furthermore, IgE activated macrophages by enhancing Na + /H + exchanger 1 (NHE1) activity. Inactivation of NHE1 blocked IgE-induced macrophage production of inflammatory molecules and apoptosis. Cultured human aortic SMCs (HuSMCs) and ECs also exhibited IgE-induced signal transduction, cytokine expression, and apoptosis. In human atherosclerotic lesions, SMCs and ECs colocalized with IgE and TUNEL staining. This study reveals what we believe to be several previously unrecognized IgE activities that affect arterial cell biology and likely other IgE-associated pathologies in human diseases.

show abstract

Section: Figurementioning

confidence: 99%

IgE stimulates human and mouse arterial cell apoptosis and cytokine expression and promotes atherogenesis in Apoe–/– mice

et al. 2011

View full text Add to dashboard Cite

show abstract

“…IgE-deficient mice possess similar numbers of CD23 + B cells as wild-type mice, but have significantly reduced levels of CD23 surface expression. The levels of CD23 can be enhanced by intravenous administration of IgE alone, mirroring findings in parasitized mice (which display high levels of serum IgE) that CD23 expression is elevated and can be reduced by anti-IgE treatment [11]. CD23 may provide a negative feedback loop in the regulation of IgE synthesis because CD23-deficient mice have higher levels of IgE production whereas CD23 transgenic mice produce less than wild-type mice [12,13].…”

Section: Historymentioning

confidence: 86%

Antigen-independent effects of immunoglobulin E

Bryce

Oettgen

2005

Curr Allergy Asthma Rep

View full text Add to dashboard Cite

Immunoglobulin E (IgE) is an important mediator in immediate hypersensitivity, as it facilitates mast cell degranulation and the release of immunomodulatory mediators, such as histamine, prostaglandins, and cytokines. Antigen-specific IgE is a hallmark of allergic diseases. Upon interaction with polyvalent antigen, IgE molecules crosslink and transmit signals that drive this process. Recently, an alternative function of IgE has come to light. Rather than merely priming the mast cell, in the absence of antigen, IgE influences mast cells, including their survival, receptor expression, and mediator release. The mechanisms by which IgE induces these effects and the biological consequences are being discovered and are showing that IgE has an important and active role in facilitating immune responses.

show abstract

“…Following anti-IgE treatment, despite undetectable levels of IgE, there was a reduced parasite burden in mice infected with P. westermani (34), and decreases in the number of adult worms and the number of eggs produced per worm in mice infected with S. mansoni (35). The protective effect of anti-IgE in these models may be on account of suppression of nonspecific IgE levels leading to more parasite-specific and focused immune response (34) or enhanced IgE-dependent cellular cytotoxicity to parasitic worms mediated by superior binding of parasiteattached IgE to FceRII/CD23 on macrophages and eosinophils. Parasite burdens during experimental infections with S. ratti were, however, not affected by anti-IgE treatment (36), and there was some evidence for an increase in survival of L3 stage O. volvulus larvae after treatment with anti-IgE (37).…”

Section: Effect Of Anti-ige Treatment In Animal Models Of Helminth Inmentioning

confidence: 99%

Geohelminth infections: a review of the role of IgE and assessment of potential risks of anti‐IgE treatment

Cooper

Ayre

Martin

et al. 2008

Allergy

View full text Add to dashboard Cite

Geohelminth infections are major parasitic infections with a worldwide distribution. Immunoglobulin E (IgE) is considered to play a central role in protective immunity against these parasites although the evidence from experimental animal models infected with helminth parasites and treated with anti‐IgE antibodies and from observational studies in human populations of the immunologic correlates of protective immunity against helminths do not support a critical role for IgE in mediating protection against helminths. Anti‐IgE treatment of human allergic disorders using a humanized monoclonal IgE antibody (omalizumab, Xolair) has been approved for clinical use in the USA and Europe and there is concern that this treatment may be associated with increased morbidity in populations exposed to helminth infections. A recently published randomized controlled trial investigating the risk of geohelminth infections in allergic patients receiving omalizumab in Brazil has provided some evidence that omalizumab may not be associated with increased morbidity attributable to these parasites. This review examines the evidence for a role of IgE in protective immunity against helminth parasites, discusses the findings of the randomized controlled trial, assesses the potential risks and provides recommendations for anti‐IgE treatment in groups of allergic patients with different exposure risks for helminth infections.

show abstract

Effects of anti-IgE mAb on serum IgE, FcεRII/CD23 expression on splenic B cells and worm burden in mice infected with Paragonimus westermani

Cited by 8 publications

References 25 publications

IgE stimulates human and mouse arterial cell apoptosis and cytokine expression and promotes atherogenesis in Apoe–/– mice

IgE stimulates human and mouse arterial cell apoptosis and cytokine expression and promotes atherogenesis in Apoe–/– mice

Antigen-independent effects of immunoglobulin E

Geohelminth infections: a review of the role of IgE and assessment of potential risks of anti‐IgE treatment

Contact Info

Product

Resources

About