The high-affinity IgE receptor (FcεRI) blocks apoptosis in normal human monocytes

Katoh, Norito; Kraft, Stefan; Wessendorf, J; Bieber, Thomas

doi:10.1172/jci6895

Cited by 86 publications

(91 citation statements)

References 46 publications

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“…nasal administration, sublingual administration) induces high IgE boosts [44,64]. The induction of allergen-specific IgE antibodies during SIT is unwanted because it is known that increased IgE antibody levels up-regulate receptors for IgE on mast cells, basophils and APCs and prolong their survival, which consecutively cause increases of allergen sensitivity in the target organs of allergy [65][66][67][68].…”

Section: Factors Limiting the Broad Application Of Allergen-specific mentioning

confidence: 99%

Developments in allergen‐specific immunotherapy: from allergen extracts to allergy vaccines bypassing allergen‐specific immunoglobulin E and T cell reactivity

Focke

Swoboda

Marth

et al. 2010

Clin Experimental Allergy

101

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SummaryAllergen-specific immunotherapy (SIT) is the only specific and disease-modifying approach for the treatment of allergy but several disadvantages have limited its broad applicability. We argue that the majority of the possible disadvantages of SIT such as unwanted effects, poor efficacy and specificity as well as inconvenient application are related to the poor quality of natural allergen extracts, which are the active ingredients of all currently available allergy vaccines. Because of the progress made in the field of molecular allergen characterization, new allergy vaccines based on recombinant allergens, recombinant hypoallergenic allergen derivatives and allergen-derived T cell peptides have entered clinical testing and hold promise to reduce the side-effects and to increase the specificity as well as the efficacy of SIT. Here, we present a refined immunotherapy concept, which is based on the use of peptides derived from allergen surfaces that exhibit reduced, allergen-specific IgE as well as T cell reactivity. These peptides when fused to non-allergenic carriers give rise to allergen-specific protective IgG responses with T cell help from a non-allergenic carrier molecule. We summarize the experimental data demonstrating that such peptide vaccines can bypass allergen-specific IgE as well as T cell activation and may be administered at high doses without IgE-and T cell-mediated side-effects. Should these peptide vaccines prove efficacious and safe in clinical trials, it may become possible to develop convenient, safe and broadly applicable forms of SIT as true alternatives to symptomatic, drug-based allergy treatment.

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Section: Factors Limiting the Broad Application Of Allergen-specific mentioning

confidence: 99%

Developments in allergen‐specific immunotherapy: from allergen extracts to allergy vaccines bypassing allergen‐specific immunoglobulin E and T cell reactivity

Focke

Swoboda

Marth

et al. 2010

Clin Experimental Allergy

101

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“…[45][46][47][48][49] In contrast to neutrophils and eosinophils, the application of survival signals to mature monocyte/macrophages results in increased expression of BCL2 and BCLX, but not MCL1. 50,51 In sum, the combination of BCL2 family members operating in the various windows along the differentiation continuum depends upon cell type and differentiation stage, as well as upon cytokine stimulation. Just as MCL1 expression can be increased by factors that promote cell viability, it is often decreased by agents that cause cell death (eg sodium salicylate and etoposide 7,52 ).…”

Section: Induction Of Mcl1 By Specific Growth and Differentiation Sigmentioning

confidence: 99%

MCL1 provides a window on the role of the BCL2 family in cell proliferation, differentiation and tumorigenesis

2002

Leukemia

252

245

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The MCL1 gene (myeloid cell leukemia-1) was discovered serendipitously about a decade ago and proved to be a member of the emerging BCL2 gene family. Ongoing studies of this gene provide an interesting perspective on the role of the BCL2 family in transitions in cell phenotype. Specifically, gene products that influence cell viability as a major effect (eg MCL1, BCL2 and other family members) can act as key determinants in cell proliferation, differentiation and tumorigenesis. Although they do not have a direct role in proliferation/differentiation programs, these genes can either permit these programs to proceed or prevent them. Through such effects, the BCL2 family regulates the normal flow of cells through cycles of proliferation and along various pathways of differentiation. A model is presented suggesting that this is accomplished by sustaining or inhibiting viability at critical points in the cell lifecycle. These critical points represent windows of time during which cell fate transitions are effected. They can also be visualized as windows that open or close to promote or prevent continued progression along various cell fate pathways. The pattern of BCL2 family expression at these points allows for the proliferation differentiation, and continued viability of cell types that are needed, while aborting these processes for cells that are overabundant or no longer needed. The combined action of the various family members can therefore control the fate of cells, tissues and even the organism. This mechanism involving apoptosis-related genes is readily executable, and is poised to respond to external signals through the differential regulation of BCL2 family members. As such, it plays an important role in the maintenance of tissue homeostasis and function. Alterations that affect the BCL2 family impair the capacity to control the flow of cells through these critical points, and thereby 'leave the window open' for cell immortalization and cancer. Targeting this family may thus provide a means of inhibiting cancer development and inducing apoptosis in tumor cells. Leukemia (2002) 16, 444-454. DOI: 10.1038/sj/leu/2402416 Keywords: MCL1; BCL2; apoptosis; differentiation; hematopoiesis; cancer MCL1 was discovered based on increased expression during cell commitment to differentiation MCL1 was originally identified as a gene up-regulated early in the differentiation of a human myeloid leukemia cell line, ML-1. 1 These cells proliferate at an immature myeloblastic stage and undergo terminal differentiation to non-proliferative monocyte/macrophages upon exposure to phorbol esters such as 12-0-tetradecanoylphorbol 13-acetate (TPA). Commitment to differentiation occurs rapidly -within a window of several hours -upon the application of TPA to growth-arrested cells. 2 The 'commitment window' precedes phenotypic differentiation, which proceeds over the next several days. ML-1 cells that have passed through the commitment window do not difCorrespondence: RW Craig, Department of Pharmacology and Toxicology, Dartmouth Medic...

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“…In particular, it is not known whether IgE sensitization through Fc⑀RI alone mediates ASM cell survival, as was demonstrated in mast cells (4,56,64) and monocytes (58), which may influence cell growth and or proliferation. The factors that influenced Fc⑀RI and Fc⑀RII expression and the contribution of each Fc⑀R in ASM cell function within the airways, e.g., airway hyperresponsiveness and inflammation, have not been investigated.…”

Section: Fc⑀ri Induced Cytokine and Chemokine Release In Asm Cellsmentioning

confidence: 99%

The high-affinity IgE receptor (FcεRI): a critical regulator of airway smooth muscle cells?

Gounni

2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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The high-affinity IgE receptor (FcεRI) blocks apoptosis in normal human monocytes

Cited by 86 publications

References 46 publications

Developments in allergen‐specific immunotherapy: from allergen extracts to allergy vaccines bypassing allergen‐specific immunoglobulin E and T cell reactivity

Developments in allergen‐specific immunotherapy: from allergen extracts to allergy vaccines bypassing allergen‐specific immunoglobulin E and T cell reactivity

MCL1 provides a window on the role of the BCL2 family in cell proliferation, differentiation and tumorigenesis

The high-affinity IgE receptor (FcεRI): a critical regulator of airway smooth muscle cells?

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