A novel anti‐apoptotic role for apolipoprotein L2 in IFN‐γ‐induced cytotoxicity in human bronchial epithelial cells

  title={A novel anti‐apoptotic role for apolipoprotein L2 in IFN‐$\gamma$‐induced cytotoxicity in human bronchial epithelial cells},
  author={Wupeng Liao and Fera Yiqian Goh and Richard J Betts and David M Kemeny and John Kit Chung Tam and Boon Huat Bay and W S Fred Wong},
  journal={Journal of Cellular Physiology},
Airway epithelium functions not only as a physical barrier, but also a regulator of lung inflammation. IFN‐γ plays a critical role in airway inflammation associated with respiratory viral infection. We investigated differential protein profiling in IFN‐γ‐stimulated normal human bronchial epithelial cells (HBEC) using a 2‐dimensional gel electrophoresis followed by MALDI‐TOF‐MS/MS. IFN‐γ markedly stimulated apolipoprotein L2 (ApoL2) protein expression in normal HBEC. ApoL2 mRNA expression was… 
Cellular inhibitor of apoptosis-2 is a critical regulator of apoptosis in airway epithelial cells treated with asthma-related inflammatory cytokines
The results indicate that AECs possess endogenous mechanisms making them highly resistant to apoptosis due to asthma‐related inflammatory cytokines, and the activity of cIAP2 plays an important role in this protection.
Apolipoproteins L control cell death triggered by TLR3/TRIF signaling in dendritic cells
It is proposed that ApoLs are involved in cell death linked to activation of DCs by viral stimuli, particularly the viral mimetic polyinosinic:polycytidylic acid (poly(I:C).
Polyopes affinis Suppressed IFN-γ- and TNF-α-Induced Inflammation in Human Keratinocytes via Down-Regulation of the NF-κB and STAT1 Pathways
The existence of phloroglucinol, a polyphenol formed from a precursor called phlorotannin, which is present in PAB is confirmed, and this result proved the possibility of PAB being used as a treatment for AD.
Long-term cigarette smoke exposure dysregulates pulmonary T cell response and IFN-γ protection to influenza virus in mouse
It is demonstrated that prior CS exposure caused a biphasic T cell and IFN-γ response to subsequent infection with influenza in the lung, and the result suggested that CS affected the kinetics of the T cell response to IAV, which was suppressed at an early stage and exaggerated at a later stage.
Apolipoprotein L2 contains a BH3-like domain but it does not behave as a BH3-only protein
In an in-silico screening to discover novel putative BH3-only proteins, this work identified yet another member of the apolipoprotein L family, apoL2 (ApoL2), as a BH 3 motif-containing protein, which, in contrast to what has been described about its homologs ApoL1 and Apo l6, did not regulate autophagy.
STAT3 Targets Suggest Mechanisms of Aggressive Tumorigenesis in Diffuse Large B-Cell Lymphoma
Examination of the affected genes identified previously undetected and clinically significant pathways downstream of STAT3 that drive oncogenesis, and novel treatments aimed at these pathways may increase the survivability of activated B-cell−like diffuse large B- cell lymphoma.
ApolipoproteinL1 is expressed in papillary thyroid carcinomas.


Dendritic cell‐derived interferon‐γ‐induced protein mediates tumor necrosis factor‐α stimulation of human lung fibroblasts
Dendritic cell‐derived interferon‐γ‐induced protein (DCIP) was upregulated by TNF‐α in lung fibroblasts and its biological function is at present unknown, and DCIP‐selective antisense oligodeoxynucleotide inhibited the expression of T NF‐α‐responsive gene targets including vascular cell adhesion molecule‐1, intercellular adhesion molecules‐1 and IL‐6, IL‐8, IP‐10.
Interferon-γ and tumor necrosis factor-α sensitize primarily resistant human endometrial stromal cells to Fas-mediated apoptosis
It is shown that ESCs are primarily resistant to Fas-mediated apoptosis independently of their state of hormonal differentiation, and the observed pro-apoptotic effect of IFN-γ and TNF-α on ESCs could play an important role in the modulation of early implantation.
Aryl Hydrocarbon Receptor Activation during Influenza Virus Infection Unveils a Novel Pathway of IFN-γ Production by Phagocytic Cells1
The lung contains important targets of AhR regulation, which likely influence a novel iNOS-mediated mechanism that controls IFN-γ production by phagocytic cells, which suggests that AhR activation changes the response of lung parenchymal cells, such that regulatory pathways in the lung are cued to respond inappropriately during infection.
The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-γ-induced cell death
It is shown that Irgm1 also regulated the survival of mature effector CD4+ T lymphocytes by protecting them from IFN-γ-induced autophagic cell death, and identified a feedback mechanism in the T helper type 1 response that limits the detrimental effects of IFn-γ on effector T lymphocyte survival while promoting the antimicrobial functions of IFN -γ.
STAT1 Activation Causes Translocation of Bax to the Endoplasmic Reticulum during the Resolution of Airway Mucous Cell Hyperplasia by IFN-γ1
Observations suggest that STAT1-dependent translocation of Bax to the ER is crucial for IFN-γ-induced cell death of AECs and the resolution of allergen-induced mucous cell hyperplasia.
Response to Comment on “Characterization of Human Lung Tumor-Associated Fibroblasts and Their Ability to Modulate the Activation of Tumor-Associated T Cells”
TAF in human NSCLC are functionally and phenotypically heterogeneous and provide multiple complex regulatory signals that have the potential to enhance or suppress TAT function in the tumor microenvironment.
Mucosal IL-10 and TGF-beta play crucial roles in preventing LPS-driven, IFN-gamma-mediated epithelial damage in human colon explants.
It is demonstrated that IL-10 ablation leads to an endogenous IFN-gamma-mediated inflammatory response via LPS from commensal bacteria in the human colonic mucosa, and it is found that bothIL-10 and TGF-beta play crucial roles in maintaining human colonIC mucosa homeostasis.
IFNγ-dependent, spontaneous development of colorectal carcinomas in SOCS1-deficient mice
Data strongly suggest that SOCS1 is a unique antioncogene which prevents chronic inflammation-mediated carcinogenesis by regulation of the IFNγ/STAT1 pathways.
Roles of apoptosis in airway epithelia.
  • Y. Tesfaigzi
  • Biology, Medicine
    American journal of respiratory cell and molecular biology
  • 2006
In the airway epithelium apoptosis serves three main roles: to eliminate damaged cells; to restore homeostasis following hyperplastic changes; and to control inflammation, and thereby support the barrier and anti-inflammatory functions.