Short-termed expression of interleukin-12 during experimental BLV infection may direct disease progression to persistent lymphocytosis
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Updated: Oct 25, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
B Yakobson1, J Brenner, H Ungar-Waron
1Department of Immunology, Kimron Veterinary Institute, Beit-Dagan, Israel.
Insights
This study reveals how cattle infected with bovine leukemia virus (BLV) mount an immune response. Early cell-mediated immunity shifts to a later IL-10 driven humoral response, influencing disease progression.
Area of Science:
- Veterinary Immunology
- Virology
- Molecular Biology
Background:
- Bovine leukemia virus (BLV) causes persistent lymphocytosis (PL+) in cattle.
- Understanding the cellular immune response to BLV is crucial for disease management.
Purpose of the Study:
- To elucidate cytokine expression during experimental BLV infection in cattle.
- To correlate cytokine profiles with disease progression stages.
Main Methods:
- Monitoring BLV infection using BLV gp51 mRNA expression and PCR/RT-PCR.
- Detecting antibodies via agar gel immuno-diffusion (AGID) test.
- Quantifying cytokine mRNA expression (IL-12p40, TNFalpha, IL-1beta, IFNgamma, IL-2, IL-10) in peripheral blood mononuclear cells (PBMCs).
Main Results:
- Antibodies detected at 5 weeks; PL+ established by 24 weeks.
- Initial IL-12p40 expression observed 1-3 weeks post-infection.
- Pro-inflammatory and cellular cytokines (TNFalpha, IL-1beta, IFNgamma, IL-2) detected from week 2-3.
- IFNgamma decreased by week 12, while IL-10 increased and persisted.
Conclusions:
- BLV infection induces a transient cell-mediated immune response (IL-12p40, IFNgamma).
- A shift towards an IL-10 mediated humoral response occurs early in infection.
- Altered cytokine balance may drive disease progression to the persistent lymphocytosis stage.
Abstract:
In this study an attempt was made to elucidate cellular response cytokine expression upon experimental bovine leukemia virus (BLV) infection in cattle. Progression of infection was monitored by BLV gp51 mRNA expression or DNA amplification by RT-PCR or PCR, respectively, to detect provirus infected cells. Antibodies to BLV were detected by an agar gel immuno-diffusion (AGID) test in 5 weeks and persistent lymphocytosis (PL+) was established in all four BLV-infected animals in 24 weeks after infection. At the initial stage of infection a strong cellular immune response was induced mediated by IL-12p40 mRNA expression. Short-termed IL-12p40 expression was observed in peripheral blood mononuclear cells (PBMC) in two out of four infected animals following 1-3 weeks after infection, while viral mRNA expression was observed 2 weeks following infection. Expression of genes coding for the pro-inflammatory TNFalpha, IL-1beta and cellular response cytokines IFNgamma and IL-2 was detected beginning with the second and third week after infection in all BLV-infected animals. However, IFNgamma expression significantly decreased in 12 weeks after infection in three animals while IL-10 message initially detected 3 weeks after infection increased by 12 weeks and persisted. The observed immediate short-termed cell mediated immune response characterized by IL-12p40 and IFNgamma expression followed by an early shift to an IL-10 induced humoral response, may change the cytokine balance and direct disease progression to the PL+ stage.
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