AI Article Synopsis

  • The discovery of tumor antigens like D393-CD20 is crucial for developing new cancer diagnostics and therapies.
  • CD8+ T lymphocytes are key players in the immune response against cancer, and this study focuses on using them against the D393-CD20 antigen in the RAMOS cell line.
  • The findings indicate that TCD8+ lymphocytes targeting D393-CD20 can effectively induce apoptosis in malignant B-lymphocytes, suggesting its potential as a target for immunotherapy.

Article Abstract

The effective discovery of clinically relevant tumor antigens holds a fundamental role for the development of new diagnostic tools and anticancer immunotherapies. D393-CD20 mRNA is absent from normal resting B cells but present in various malignant or transformed B cells. CD8+T lymphocytes play a central role in immunity to cancer. In this study, we want use from T CD8+ against D393-CD20 for effect in RAMOS cell line. After isolation and expanding of specific TCD8 + Lymphocyte against D393-CD20 antigen, for examining the effect of specialized T lymphocyte clone of D393-CD20 antigen on RAMOS cell line, we co-cultured them together, and the rate of apoptosis were examined by flow cytometry and cytotoxicity techniques by using MTT technique. We observed that specialized TCD8+ lymphocyte of D393-CD20 antigen can induce apoptosis in malignant B-lymphocytes, and this antigen can be a proper target for immunotherapy.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6852797PMC
http://dx.doi.org/10.31557/APJCP.2019.20.8.2563DOI Listing

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Article Synopsis
  • The discovery of tumor antigens like D393-CD20 is crucial for developing new cancer diagnostics and therapies.
  • CD8+ T lymphocytes are key players in the immune response against cancer, and this study focuses on using them against the D393-CD20 antigen in the RAMOS cell line.
  • The findings indicate that TCD8+ lymphocytes targeting D393-CD20 can effectively induce apoptosis in malignant B-lymphocytes, suggesting its potential as a target for immunotherapy.
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CD20 alternative splicing isoform generates immunogenic CD4 helper T epitopes.

Int J Cancer

July 2015

INSERM UMR1098, F25020 Besançon cedex, France; Université de Franche-Comté, F25020 Besançon cedex, France; EFS Bourgogne Franche-Comté, F25020 Besançon cedex, France.

Cancer-specific splice variants gain significant interest as they generate neo-antigens that could be targeted by immune cells. CD20, a membrane antigen broadly expressed in mature B cells and in B cell lymphomas, is subject to an alternative splicing named D393-CD20 leading to loss of membrane expression of the spliced isoform. D393-CD20 expression is detectable in transformed B cells and upregulated in various lymphoma B cells.

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The need for markers and predictors of Rituximab treatment resistance.

Exp Dermatol

April 2014

Department of Dermatology, University Medical Center Freiburg, Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, Freiburg, Germany; Department of Rheumatology and Clinical Immunology, Center for Chronic Immunodeficiency, University Medical Center Freiburg, Freiburg, Germany.

CD20-specific antibodies show remarkable therapeutic efficacy in B-cell malignancy and autoimmune diseases, but due to the occurrence of a significant treatment resistance, a critical, unmet need for improving B-cell-depleting approaches remains. A CD20 transcript variant (D393-CD20) appears to be associated with Rituximab treatment resistance in malignant B cells, but is lacking in patients with autoimmune dermatoses as shown by Gamonet et al. While CD20-specific factors certainly play a major role in the pathogenesis of Rituximab treatment resistance, the D393-CD2 transcript may greatly facilitate the development of clinical markers for monitoring the therapy in B-cell malignancies and (auto)antibody-mediated diseases.

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We have identified a spliced mRNA transcript of CD20 (named D393-CD20) which was associated with resistance to RTX in primary B cell from patients with lymphoma and leukaemia. In the present work, we wished to investigate whether D393-CD20 variant was expressed by B cells from patients with pemphigus. Ten patients with bullous pemphigoid and twenty-five patients with pemphigus were included.

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