We developed a unique fusion partner cell line that is capable of fusing with both human peripheral blood and lymph node lymphocytes at a high efficiency. The cell line was generated by fusing a murine myeloma cell line with a human myeloma cell line, producing a heteromyeloma (B6B11), which was subsequently fused with a human lymph node lymphocyte to produce a trioma (MFP-2). B6B11 and MFP-2 fuse well with human lymphocytes from both spleen and lymph nodes. Interestingly, MFP-2 also fuses with a high efficiency to peripheral blood lymphocytes. The resulting hybrids are stable for extended periods of time and produce human monoclonal antibodies at significant levels. The utility of MFP-2 as a fusion partner was demonstrated by the isolation of several hybridoma cell lines using lymph node and peripheral blood lymphocytes from patients with breast cancer. These hybridomas produce monoclonal antibodies displaying specificity to breast cancer tissue and cell lines.

Download full-text PDF

Source

Publication Analysis

Top Keywords

peripheral blood
16
fusion partner
12
monoclonal antibodies
12
blood lymphocytes
12
lymph node
12
partner cell
8
human monoclonal
8
high efficiency
8
myeloma cell
8
cell lines
8

Similar Publications

Therapeutic gene correction of HBB frameshift CD41-42 (-TCTT) deletion in human hematopoietic stem cells.

Adv Biotechnol (Singap)

January 2025

MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, 510275, Guangdong, China.

Β-thalassemia is one of the global health burdens. The CD41-42 (-TCTT) mutation at HBB is the most prevalent pathogenic mutation of β-thalassemia in both China and Southeast Asia. Previous studies focused on repairing the HBB CD41-42 (-TCTT) mutation in β-thalassemia patient-specific induced pluripotent stem cells, which were subsequently differentiated into hematopoietic stem and progenitor cells (HSPCs) for transplantation.

View Article and Find Full Text PDF

Adenine base editor corrected ADPKD point mutations in hiPSCs and kidney organoids.

Adv Biotechnol (Singap)

June 2024

MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, 510275, China.

Autosomal dominant polycystic kidney disease (ADPKD) is a dominant genetic disorder caused primarily by mutations in the PKD1 gene, resulting in the formation of numerous cysts and eventually kidney failure. However, there are currently no gene therapy studies aimed at correcting PKD1 gene mutations. In this study, we identified two mutation sites associated with ADPKD, c.

View Article and Find Full Text PDF

Enzyme-linked immunosorbent spot analysis is frequently used to investigate immune responsiveness during clinical trials. However, ELISpot classically utilizes peripheral blood mononuclear cell isolates from whole blood, requiring relatively high blood draw volumes and removing both granulocytes and bound drug. Here, we describe a novel protocol whereby CD45 cells are magnetically isolated from human whole blood and co-incubated with serum isolated from the same subject.

View Article and Find Full Text PDF

Peripheral neuropathy is a complication in systemic sclerosis that is occasionally encountered in clinical settings. The mechanisms underlying this condition remain unclear and treatment strategies have not yet been established, making management challenging. Here, we report a case of peripheral neuropathy associated with systemic sclerosis that was successfully treated with corticosteroid therapy despite the absence of conventional inflammatory findings on histopathology or blood tests.

View Article and Find Full Text PDF

Intracerebral hemorrhage (ICH) is the most common subtype of hemorrhagic stroke causing significant morbidity and mortality. Previously clinical treatments for ICH have largely been based on a single pathophysiological perspective, and there remains a lack of curative interventions. Following the rupture of cerebral blood vessels, blood metabolites activate resident immune cells such as microglia and astrocytes, and infiltrate peripheral immune cells, leading to the release of a series of inflammatory mediators.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!