Dataset Information

Quantitative proteomics of non hodgkin's

ABSTRACT: Abstract: ArtinM, a D-mannose-binding lectin from Artocarpus heterophyllus induces the activation of a Mast cell, neutrophils, macrophages, and CD4+ and CD8+ T cells, via carbohydrate recognition. we previously reported, that ArtinM is able to induce IL-17 and IL-12p40 production in murine B cells. Here, we further investigated the effects of ArtinM on murine B lymphocytes and Raji and Daudi cells, both human cell lines derived from non-Hodgkin lymphoma. We showed that ArtinM did not induce cell proliferation and low levels of IL-2, IFN-γ, and IL-12 were produced by murine B cells. However, high concentrations of ArtinM induced apoptosis of murine B cells. Then, evaluated the cytotoxic effect of ArtinM lectin against Raji and Daudi cells. we observed the ArtinM ability to reduce cell growth and cell viability, with a more pronounced cytotoxic effect on Raji cells. In addition, we observed the absence of DNA fragmentation, a strong indication of the exclusion of the apoptosis cascade via mitochondrial pathway, and the possible involvement of PTK, kinases of Src family, and CD45 phosphatase activity under Lck molecule in the cytotoxic effect of ArtinM in the Raji and Daudi cells. Thus, the present work demonstrates the limitations of the immunomodulatory effect of ArtinM under murine B cells, and provides insights in the investigative field in the non-Hodgkin lymphoma treatment, via carbohydrate recognition.

INSTRUMENT(S): Synapt MS

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): B Cell, Cell Suspension Culture

DISEASE(S): Lymphoma

SUBMITTER: Alexandre Keiji Tashima

LAB HEAD: Alexandre Keiji Tashima

PROVIDER: PXD029399 | Pride | 2023-03-11

REPOSITORIES: Pride

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ArtinM Cytotoxicity in B Cells Derived from Non-Hodgkin's Lymphoma Depends on Syk and Src Family Kinases.

Barboza Bruno Rafael BR Thomaz Sandra Maria de Oliveira SMO Junior Airton de Carvalho AC Espreafico Enilza Maria EM Miyamoto Jackson Gabriel JG Tashima Alexandre Keiji AK Camacho Maurício Frota MF Zelanis André A Roque-Barreira Maria Cristina MC da Silva Thiago Aparecido TA

International journal of molecular sciences 20230105 2

Receptors on the immune cell surface have a variety of glycans that may account for the immunomodulation induced by lectins, which have a carbohydrate recognition domain (CRD) that binds to monosaccharides or oligosaccharides in a specific manner. ArtinM, a D-mannose-binding lectin obtained from Artocarpus heterophyllus, has affinity for the N-glycans core. Immunomodulation by ArtinM toward the Th1 phenotype occurs via its interaction with TLR2/CD14 N-glycans on antigen-presenting cells, as well ...[more]

PMID: 36674590

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Project description:Background Epigenetic changes are involved in the extinction of the B-cell gene expression program of classical Hodgkin lymphoma. However, little is known regarding epigenetic similarities between classical Hodgkin lymphoma and plasma cell myeloma cells, both of which share an extinction of the gene expression program of mature B-cells. Design and methods Global histone H3 acetylation patterns were determined in cell lines derived from classical Hodgkin lymphoma, plasma cell myeloma and B-cell lymphoma by chromatin immunoprecipitation and subsequent hybridization onto promoter tiling arrays. H3K27 trimethylation was analyzed by chromatin immunoprecipitation and real-time DNA-PCR for selected genes. Epigenetic modifications were compared to gene expression data. Results B-cell characteristic genes were hypoacetylated in classical Hodgkin lymphoma and plasma cell myeloma cell lines, as demonstrated by comparison of their histone H3 acetylation patterns to those of B-cell lines. However, the number of genes jointly hyperacetylated and expressed in classical Hodgkin lymphoma and plasma cell myeloma cell lines, such as IFR4/MUM1 and RYBP, is limited. Moreover, H3K27 trimethylation for selected B-cell characteristic genes revealed that this additional epigenetic silencing is much more prevalent in classical Hodgkin lymphoma as compared to plasma cell myeloma. Conclusion Our epigenetic data support the view that classical Hodgkin lymphoma is characterized by an abortive plasma cell differentiation with a down-regulation of B-cell characteristic genes but without activation of most plasma cell typical genes. Combined 5-aza-dC/TSA (A/T) treatment: The diffuse large B-cell lymphoma (DLBCL)-derived cell lines SU-DHL4, SU-DHL6 and HT and the Burkitt lymphoma-derived cell lines Daudi, Namalwa and Raji were treated with 5-aza-dC at a concentration of 3 µM for 6 days. 5-aza-dC and medium was replaced at day 2 and 5. At the fifth day - in addition to 3 µM 5-aza-dC - cells were incubated for 24 hours with 625 nM TSA. RNA was isolated according to standard protocols (Qiagen, Hilden, Germany) and used for Affymetrix GeneChip hybridization (HG-U133A). Microarrays were normalized using RMA and differential expression was calculated using moderated t-test. The gene expression profiles of the untreated and treated cell lines (with the exception of HT) were generated in duplicates. Microarray data (CEL files) for AZA/TSA-treated BL-derived cell lines Raji, Daudi and Namalwa were previously published (GEO accession GSE8388).

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