Related Experiment Video
Updated: Aug 9, 2026
Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
Published on: January 7, 2019
Modulation of bovine leukemia virus-associated spontaneous lymphocyte proliferation by monoclonal antibodies to
D M Stone1, L K Norton, W C Davis
1Department of Veterinary Microbiology and Pathology, Washington State University, Pullman 99164-7040, USA.
Insights
Bovine leukemia virus (BLV) infection causes abnormal lymphocyte proliferation. Researchers found specific cell surface molecules, CD11c, MHC class I, and MHC class II, are upregulated, impacting immune cell activity.
Area of Science:
- Veterinary Immunology
- Virology
- Molecular Biology
Background:
- Human T lymphotropic virus (HTLV) and bovine leukemia virus (BLV) infections are linked to uncontrolled lymphocyte proliferation in vitro.
- Dysregulated lymphocyte activity in these infections may involve signaling pathways mediated by cell surface molecules crucial for immune regulation.
Purpose of the Study:
- To investigate the expression of adhesion and major histocompatibility (MHC) molecules on lymphocytes from BLV-infected cattle with persistent lymphocytosis.
- To determine if monoclonal antibodies targeting these surface molecules can modulate spontaneous lymphocyte proliferation.
Main Methods:
- Flow cytometry was used to analyze the expression of CD11c, MHC class I, and MHC class II molecules on lymphocytes from BLV-infected and healthy cattle.
- The effect of monoclonal antibodies against CD11c, MHC class I, and MHC class II on spontaneous lymphocyte proliferation was assessed in vitro.
Main Results:
- CD11c, MHC class I, and MHC class II molecules were found to be upregulated on both B and T lymphocytes in cattle with persistent lymphocytosis (PL).
- Anti-CD11c antibodies stimulated lymphocyte proliferation in all cows, with a more pronounced effect on lymphocytes from PL cows.
- Antibodies targeting bovine MHC class I and class II molecules inhibited spontaneous lymphocyte proliferation.
Conclusions:
- Lymphocyte dysregulation in BLV-induced persistent lymphocytosis involves the upregulation of cell surface molecules like CD11c and MHC molecules.
- Signaling through these upregulated surface molecules plays a role in the aberrant immune activation observed in BLV infection.
Abstract:
Both human T lymphotropic virus (HTLV) and bovine leukemia virus (BLV) infections are characterized by in vitro proliferation of peripheral blood lymphocytes in the absence of exogenous antigens or mitogens. Differential expression of lymphocyte surface molecules in HTLV and BLV infection suggests that lymphocyte dysregulation may involve signaling through surface molecules involved in immune regulation. We examined the expression of adhesion and major histocompatibility (MHC) molecules on circulating lymphocytes from BLV-infected cows with persistent lymphocytosis and the ability of monoclonal antibodies to these molecules to modulate spontaneous lymphocyte proliferation. The integrin molecule, CD11c, and both MHC class I and MHC class II molecules were upregulated on B and T lymphocytes from PL cows. Anti-CD11c antibody was stimulatory to lymphocyte proliferation regardless of BLV status and had a greater stimulatory effect on spontaneously proliferating lymphocytes from persistently lymphocytotic cows than on normal bovine lymphocytes. Antibodies to bovine class I and class II inhibited spontaneous lymphocyte proliferation. Results suggest that lymphocyte dysregulation in BLV-induced persistent lymphocytosis involves upregulation of and signaling through lymphocyte surface molecules which are involved in immune activation of lymphocytes.
Related Concept Videos
01:31Hybridoma Technology
Hybridoma Selection
Commonly used fusion techniques — electroporation, polyethylene glycol...
01:24B Cell Activation and Differentiation
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...