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.

Highlights

  • CD8+T lymphocytes play a central role in immunity to cancer through their capacity to kill malignant cells upon recognition by T-cell receptor (TCR) of specific antigenic peptides presented on the surface of target cells by human leukocyte antigen class I (HLA-I)/beta-2-microglobulin (β2m) complexes (Bossi et al, 2002)

  • After staining some of the selected T lymphocyte clone cells of D393-CD20 antigen with Anti CD4 connected to FITC stain and Anti CD8 connected to PE, by using flow cytometry device, it was determined that 86.6% of selected cell populations were CD8+ and CD4

  • Results of MTT test related to RAMOS cell line co-cultured with specialized T lymphocytes of D393-CD20 antigen

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Summary

Introduction

CD8+T lymphocytes play a central role in immunity to cancer through their capacity to kill malignant cells upon recognition by T-cell receptor (TCR) of specific antigenic peptides presented on the surface of target cells by human leukocyte antigen class I (HLA-I)/beta-2-microglobulin (β2m) complexes (Bossi et al, 2002). Evidence for antitumor CD8+T-cell immunity was provided by isolation of tumor-specific CTL from peripheral blood or tumor tissue of patients with diverse cancers, such as melanoma and lung carcinoma (Boon et al.,1997; Echchakir et al, 2000; Karanikas, 2001; Slingluff et al.,1994; Weynants et al, 1999). Aside from its role in physiological cell adaptation, alternative splicing has been shown to occur in human diseases, including cancer (Kaida et al, 2012). Cancer-specific splice variants are of significant interest as they may be involved in pathogenesis and may further potentially be used as biomarkers and generate novel targets for therapy

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