A proteomics approach to elucidate the role of Nrf2 in primary bone-marrow-derived dendritic cells of mice upon activation by contact allergens

2014 ◽  
Vol 229 ◽  
pp. S203
Author(s):  
Franz Mussotter ◽  
Andrea Haase ◽  
Janina Melanie Tomm ◽  
Zeina El Ali ◽  
Saadia Kerdine-Römer ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Contact Allergens ◽  
Proteomics Approach ◽  
Primary Bone ◽  
Primary Bone Marrow

A proteomics approach to elucidate the role of the KEAP1/NRF2 pathway in dendritic cells upon activation by chemical contact allergens

2011 ◽  
Vol 205 ◽  
pp. S148
Author(s):  
A. Haase ◽  
F. Mussotter ◽  
Z. El-Ali ◽  
S. Kerdine-Roemer ◽  
C. Wruck ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Contact Allergens ◽  
Nrf2 Pathway ◽  
Proteomics Approach

scholarly journals Characterization of Murine Dendritic Cell Line JAWS II and Primary Bone Marrow-Derived Dendritic Cells in Chlamydia muridarum Antigen Presentation and Induction of Protective Immunity

2008 ◽  
Vol 76 (6) ◽  
pp. 2392-2401 ◽  
Author(s):  
Xiaozhou Jiang ◽  
Caixia Shen ◽  
Jose Rey-Ladino ◽  
Hong Yu ◽  
Robert C. Brunham
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Antigen Presentation ◽  
Cell Line ◽  
Interleukin 12 ◽  
Developmental Cycle ◽  
Activation Markers ◽  
Chlamydia Muridarum ◽  
Primary Bone ◽  
Primary Bone Marrow

ABSTRACT Dendritic cells (DCs) appear to orchestrate much of the immunobiology of Chlamydia infection, but most studies of Chlamydia-DC interaction have been limited by the availability and heterogeneity of primary bone marrow-derived DCs (BMDCs). We therefore evaluated the immunobiology of Chlamydia muridarum infection in an immortal DC line termed JAWS II derived from BMDCs of a C57BL/6 p53-knockout mouse. JAWS II cells were permissive to the developmental cycle of Chlamydia. Infection-induced cell death was 50 to 80% less in JAWS II cells than in BMDCs. Chlamydia infected JAWS II cells and yielded infectious progeny 10-fold greater than that with primary BMDCs. JAWS II cells showed an expression pattern of cell activation markers and cytokine secretion following Chlamydia infection similar to that of primary BMDCs by up-regulating the expression of CD86, CD40, and major histocompatibility complex class II and secreting significant amounts of interleukin-12 (IL-12) but not IL-10. JAWS II cells pulsed with Chlamydia stimulated immune CD4+ T cells to secrete gamma interferon. Adoptive transfer of ex vivo Chlamydia-pulsed JAWS II cells conferred levels of immunity on C57BL/6 mice similar to those conferred by primary BMDCs. Taken together, the data show that JAWS II cells exhibit immunobiological characteristics and functions similar to those of primary BMDCs in terms of Chlamydia antigen presentation in vitro and antigen delivery in vivo. We conclude that the JAWS II cell line can substitute for primary BMDCs in Chlamydia immunobiological studies.

scholarly journals A novel imatinib-upregulated long noncoding RNA plays a critical role in inhibition of tumor growth induced by Abl oncogenes

2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Yun Ma ◽  
Guijie Guo ◽  
Tingting Li ◽  
Faxin Wen ◽  
Jianling Yang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Tumor Growth ◽  
Cell Survival ◽  
Cellular Transformation ◽  
Leukemic Cells ◽  
Transformed Cell ◽  
Primary Bone ◽  
Primary Bone Marrow ◽  
Xenografted Tumor

Abstract Background Dysregulation of long noncoding RNAs (lncRNAs) has been linked to various human cancers. Bcr-Abl oncogene that results from a reciprocal translocation between human chromosome 9 and 22, is associated with several hematological malignancies. However, the role of lncRNAs in Bcr-Abl-induced leukemia remains largely unexplored. Methods LncRNA cDNA microarray was employed to identify key lncRNAs involved in Bcr-Abl-mediated cellular transformation. Abl-transformed cell survival and xenografted tumor growth in mice were evaluated to dissect the role of imatinib-upregulated lncRNA 1 (IUR1) in Abl-induced tumorigenesis. Primary bone marrow transformation and in vivo leukemia transplant using lncRNA-IUR1 knockout (KO) mice were further conducted to address the functional relevance of lncRNA-IUR1 in Abl-mediated leukemia. Transcriptome RNA-seq and Western blotting were performed to determine the mechanisms by which lncRNA-IUR1 regulates Bcr-Abl-induced tumorigenesis. Results We identified lncRNA-IUR1 as a critical negative regulator of Bcr-Abl-induced tumorigenesis. LncRNA-IUR1 expressed in a very low level in Bcr-Abl-positive cells from chronic myeloid leukemia patients. Interestingly, it was significantly induced in Abl-positive leukemic cells treated by imatinib. Depletion of lncRNA-IUR1 promoted survival of Abl-transformed human leukemic cells in experiments in vitro and xenografted tumor growth in mice, whereas ectopic expression of lncRNA-IUR1 sensitized the cells to apoptosis and suppressed tumor growth. In concert, silencing murine lncRNA-IUR1 in Abl-transformed cells accelerated cell survival and the development of leukemia in mice. Furthermore, lncRNA-IUR1 deficient mice were generated, and we observed that knockout of murine lncRNA-IUR1 facilitated Bcr-Abl-mediated primary bone marrow transformation. Moreover, animal leukemia model revealed that lncRNA-IUR1 deficiency promoted Abl-transformed cell survival and development of leukemia in mice. Mechanistically, we demonstrated that lncRNA-IUR1 suppressed Bcr-Abl-induced tumorigenesis through negatively regulating STAT5-mediated GATA3 expression. Conclusions These findings unveil an inhibitory role of lncRNA-IUR1 in Abl-mediated cellular transformation, and provide new insights into molecular mechanisms underlying Abl-induced leukemogenesis.

Application of SILAC Labeling to Primary Bone Marrow-Derived Dendritic Cells Reveals Extensive GM-CSF-Dependent Arginine Metabolism

2013 ◽  
Vol 13 (2) ◽  
pp. 752-762 ◽  
Author(s):  
Ivo Fabrik ◽  
Marek Link ◽  
Anetta Härtlova ◽  
Vera Dankova ◽  
Pavel Rehulka ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Arginine Metabolism ◽  
Gm Csf ◽  
Primary Bone ◽  
Primary Bone Marrow

scholarly journals Primary Bone Marrow B-Cell Lymphoma Undetected by Multiple Imaging Modalities That Initially Presented with Hypercalcemia

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Jin Sae Yoo ◽  
Juwon Kim ◽  
Hyeong Ju Kwon ◽  
Jung Soo Lim
Keyword(s):  
Computed Tomography ◽  
Bone Marrow ◽  
B Cell ◽  
Cell Lymphoma ◽  
Hematologic Malignancy ◽  
B Cell Lymphoma ◽  
Severe Hypercalcemia ◽  
Multiple Imaging ◽  
Primary Bone ◽  
Primary Bone Marrow

Purpose. We report a rare case of severe hypercalcemia that was ultimately diagnosed as primary bone marrow diffuse large B-cell lymphoma (BCL). Case Report. A 74-year-old male patient visited our hospital complaining of tenderness and swelling of the left knee caused by supracondylar fracture of the left distal femur. His initial blood tests showed a serum calcium level of 13.9 mg/dL, inorganic phosphorus of 4.34 mg/dL, and a serum creatinine level of 1.54 mg/dL. A serum assay of intact parathyroid hormone showed 5.24 pg/mL, and the patient’s serum 25(OH)D level was 22.33 ng/mL. To exclude malignancy, we performed imaging studies, including abdomen or chest computed tomography and positron emission tomography-computed tomography; however, no suspicious lesion was found, although the serum PTH-related peptide level was elevated at 4.0 pmol/L. A bone marrow biopsy was performed to identify any hidden hematologic malignancy. As a result, the pathology of bone marrow confirmed the presence of atypical lymphocytes that stained positive for the CD20 marker, which is consistent with BCL involving the bone marrow. Conclusion. This case highlights the importance of pursuing a thorough workup for rare underlying causes of hypercalcemia when parathyroid-related etiologies can be excluded.

scholarly journals Rho-mDia1 pathway is required for adhesion, migration, and T-cell stimulation in dendritic cells

Blood ◽  
2010 ◽  
Vol 116 (26) ◽  
pp. 5875-5884 ◽  
Author(s):  
Hideaki Tanizaki ◽  
Gyohei Egawa ◽  
Kayo Inaba ◽  
Tetsuya Honda ◽  
Saeko Nakajima ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
T Cell ◽  
Immune Responses ◽  
Lymph Nodes ◽  
Actin Polymerization ◽  
Cell Stimulation ◽  
T Cell Stimulation ◽  
Acquired Immune Responses

Abstract Dendritic cells (DCs) are essential for the initiation of acquired immune responses through antigen acquisition, migration, maturation, and T-cell stimulation. One of the critical mechanisms in this response is the process actin nucleation and polymerization, which is mediated by several groups of proteins, including mammalian Diaphanous-related formins (mDia). However, the role of mDia in DCs remains unknown. Herein, we examined the role of mDia1 (one of the isoforms of mDia) in DCs. Although the proliferation and maturation of bone marrow-derived DCs were comparable between control C57BL/6 and mDia1-deficient (mDia1−/−) mice, adhesion and spreading to cellular matrix were impaired in mDia1−/− bone marrow–derived DCs. In addition, fluorescein isothiocyanate-induced cutaneous DC migration to draining lymph nodes in vivo and invasive migration and directional migration to CCL21 in vitro were suppressed in mDia1−/− DCs. Moreover, sustained T-cell interaction and T-cell stimulation in lymph nodes were impaired by mDia1 deficiency. Consistent with this, the DC-dependent delayed hypersensitivity response was attenuated by mDia1-deficient DCs. These results suggest that actin polymerization, which is mediated by mDia1, is essential for several aspects of DC-initiated acquired immune responses.

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