The Aml14 and Aml14.3D10 Cell Lines: A Long‐Overdue Model for the Study of Eosinophils and More

Baumann, Michael A.; Paul, Cassandra C.

doi:10.1002/stem.160016

Cited by 61 publications

(52 citation statements)

References 44 publications

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“…Following this, we tested the effect of CD5L on the proliferation of the AML14.3D10 human eosinophil cell line ( Figure 4B). The AML14.3D10 human myeloid leukemic cell line has been used as a model cell line for the study of eosinophil (Baumann and Paul, 1998;Yoon et al, 2005). Interestingly, CD5L increases the proliferation of the AML14.3D10 cell in a dose-dependent manner with IL-5 ( Figure 4C).…”

Section: Validation Of Cd5l Protein Expression Level In Ad Patients Amentioning

confidence: 98%

Glycoproteomic analysis of plasma from patients with atopic dermatitis: CD5L and ApoE as potential biomarkers

et al. 2008

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Atopic dermatitis (AD) is an inflammatory skin disorder that is both uncomfortable and distressing to patients, and its prevalence has been steadily increasing. It is obvious that the identification of efficient markers of AD in plasma would offer the possibility of effective diagnosis, prevention, and treatment strategies. In this study, a proteomic approach was used to analyze plasma glycoproteins from both children with AD and healthy child donors. Several protein spots showing significant quantitative changes in the AD patients were identified. Through sequential studies, it was confirmed that CD5L and ApoE were significantly up-regulated or down-regulated, respectively, in the plasma from AD patients compared with that from healthy donors. In addition, we suggest that the up-regulated CD5L in AD patients causes eosinophilia by inhibiting apoptosis or promoting the proliferation of eosinophils either in combination with or without IL-5. The glycoproteomic data in this study provides clues to understanding the mechanism of atopic alterations in plasma and suggests AD-related proteins can be used as candidate markers for AD.

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Section: Validation Of Cd5l Protein Expression Level In Ad Patients Amentioning

confidence: 98%

Glycoproteomic analysis of plasma from patients with atopic dermatitis: CD5L and ApoE as potential biomarkers

et al. 2008

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“…C. Paul and M. Baumann (Wright State University, Dayton, OH) (26,27). The parental AML14 cell line (pAML) was established from a patient with FAB M2 acute myeloid leukemia (26).…”

Section: Cell Culturementioning

confidence: 99%

Fas Resistance of Leukemic Eosinophils Is Due to Activation of NF-κB by Fas Ligation

Qin

Camoretti-Mercado

Blokh

et al. 2002

The Journal of Immunology

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TNF family receptors can lead to the activation of NF-κB and this can be a prosurvival signal in some cells. Although activation of NF-κB by ligation of Fas (CD95/Apo-1), a member of the TNFR family, has been observed in a few studies, Fas-mediated NF-κB activation has not previously been shown to protect cells from apoptosis. We examined the Fas-induced NF-κB activation and its antiapoptotic effects in a leukemic eosinophil cell line, AML14.3D10, an AML14 subline resistant to Fas-mediated apoptosis. EMSA and supershift assays showed that agonist anti-Fas (CH11) induced nuclear translocation of NF-κB heterodimer p65(RelA)/p50 in these cells in both a time- and dose-dependent fashion. The influence of NF-κB on the induction of apoptosis was studied using pharmacological proteasome inhibitors and an inhibitor of IκBα phosphorylation to block IκBα dissociation and degradation. These inhibitors at least partially inhibited NF-κB activation and augmented CH11-induced cell death. Stable transfection and overexpression of IκBα in 3D10 cells inhibited CH11-induced NF-κB activation and completely abrogated Fas resistance. Increases in caspase-8 and caspase-3 cleavage induced by CH11 and in consequent apoptotic killing were observed in these cells. Furthermore, while Fas-stimulation of resistant control 3D10 cells led to increases in the antiapoptotic proteins cellular inhibitor of apoptosis protein-1 and X-linked inhibitor of apoptosis protein, Fas-induced apoptosis in IκBα-overexpressing cells led to the down-modulation of both of these proteins, as well as that of the Bcl-2 family protein, Bcl-xL. These data suggest that the resistance of these leukemic eosinophils to Fas-mediated killing is due to induced NF-κB activation.

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“…for eotaxins) (51) and expresses GM-CSF, which drives its proliferation, differentiation, and survival in culture (52). The mature nature of this cell line and its utility for studies of eosinophil biology were described in a recent review (53).…”

Section: Methodsmentioning

confidence: 99%

“…The cells were collected at each time point by immediate centrifugation. In some experiments, the AML14.3D10 cells were first precultured with neutralizing anti-GM-CSF antibody for 2 days prior to stimulation with IL-5 to block autocrine signaling by GM-CSF produced by these cells in culture (52,53).…”

Section: Methodsmentioning

confidence: 99%

Engagement of the CrkL Adapter in Interleukin-5 Signaling in Eosinophils

Du¹,

Alsayed²,

Xin³

et al. 2000

Journal of Biological Chemistry

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The Aml14 and Aml14.3D10 Cell Lines: A Long‐Overdue Model for the Study of Eosinophils and More

Cited by 61 publications

References 44 publications

Glycoproteomic analysis of plasma from patients with atopic dermatitis: CD5L and ApoE as potential biomarkers

Glycoproteomic analysis of plasma from patients with atopic dermatitis: CD5L and ApoE as potential biomarkers

Fas Resistance of Leukemic Eosinophils Is Due to Activation of NF-κB by Fas Ligation

Engagement of the CrkL Adapter in Interleukin-5 Signaling in Eosinophils

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