Human Eosinophils Express Bcl-2 Family Proteins: Modulation of Mcl-1 Expression by IFN- γ

Druilhe, Anne; Arock, Michel; Goff, Liliane Le; Pretolani, Marina

doi:10.1165/ajrcmb.18.3.3019

Cited by 55 publications

(46 citation statements)

References 36 publications

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“…38,41,44 A similar principle arises out of studies in eosinophils, where the pattern of expression of MCL1 and other members of the BCL2 family appears to depend upon both the state of the cells and the type of cytokine applied. [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.…”

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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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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“…Mcl-1 expression has since been found to exhibit differentiation stage-specific expression in a variety of hematopoietic lineages as well as in epithelial tissues (19,20). In addition, Mcl-1 can be rapidly induced through anti-apoptotic cytokine-mediated pathways, such as those stimulated by hematopoietic cell colony-stimulating factors and interleukins (21)(22)(23)(24)(25). For example, in neutrophils (26), external stimuli that prolong the neutrophil life span (such as lipopolysaccharide and granulocyte-macrophage colony-stimulating factor) cause an increase in Mcl-1 expression (23,27).…”

mentioning

confidence: 99%

Exon Skipping in Mcl-1 Results in a Bcl-2 Homology Domain 3 Only Gene Product That Promotes Cell Death

Bingle¹,

Craig²,

Swales³

et al. 2000

Journal of Biological Chemistry

168

125

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“…In addition, because timing of the viral infection was not limiting, the IFN-␥-associated Th1 environment might also alter the established Th2 immune responses by affecting eosinophilic cell accumulation, survival, and/or activation. 47, 48 The combination of all of these effects could significantly impact on the outcome of the developing responses. These studies clearly demonstrate that whereas RSV can alter and predispose some mice (BALB/c) to a more severe allergic response, it also has the ability to protect other genetically different animals (C57BL/6) from a similar allergic response.…”

Section: Discussionmentioning

confidence: 99%

Respiratory Virus-Induced Regulation of Asthma-Like Responses in Mice Depends upon CD8 T Cells and Interferon-γ Production

Smit

Boon

Lukacs

2007

The American Journal of Pathology

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Respiratory virus infections can significantly influence the development of airway disease by both predisposing and exacerbating the developing lung immune environment. In contrast, the initiation of a more desirable anti-viral response may better prepare the local environment and protect it from developing an adverse long-term disease phenotype. BALB/c or C57BL/6 mice exposed to respiratory syncytial virus (RSV) infection at the same time as allergen sensitization were assessed for airway function, cytokine responses, and inflammatory parameters. Depending on the genetic strain of mouse used, BALB/c versus C57BL/6, RSV could differentially protect against the development of airway allergen responses. Although RSV was able to block allergen sensitization and induction of airway hyperresponsiveness and eosinophilic inflammation in C57BL/6 mice, the infection did not reduce the allergic responses in BALB/c mice. The alteration of airway responsiveness did not depend on the timing of RSV infection in C57BL/6 mice in conjunction to the allergen sensitization protocol. Neutralization experiments demonstrated that interferon-␥ contributed significantly to the RSV-induced airway attenuation of the allergic responses, whereas transfer of CD8 T cells from RSV-infected animals suggested that they were partially responsible for the altered environment. These data suggest that a respiratory viral infection impacts on the local lung environment and may reflect specific aspects of the hygiene hypothesis. However, the outcome of this interaction depends on the immunological response of the host.

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Human Eosinophils Express Bcl-2 Family Proteins: Modulation of Mcl-1 Expression by IFN- γ

Cited by 55 publications

References 36 publications

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

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

Exon Skipping in Mcl-1 Results in a Bcl-2 Homology Domain 3 Only Gene Product That Promotes Cell Death

Respiratory Virus-Induced Regulation of Asthma-Like Responses in Mice Depends upon CD8 T Cells and Interferon-γ Production

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