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L3T4+ T cells regulate Abelson virus-induced lymphomagenesis
A J Infante1, S Boulware, M Cagle
1Department of Pediatrics, University of Texas Health Science Center, San Antonio 78284.
Journal of Immunology (Baltimore, Md. : 1950)
|April 1, 1988
Summary
T cells, specifically L3T4+ T cells, are crucial for regulating lymphomagenesis. Depleting these cells increases susceptibility to Abelson murine leukemia virus (AMuLV)-induced lymphoma, highlighting their protective role.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- Lymphomagenesis, the development of lymphoma, is a complex process.
- Abelson murine leukemia virus (AMuLV) is a B lymphotropic retrovirus that induces lymphoma.
- The role of T cells in regulating lymphomagenesis is not fully understood.
Purpose of the Study:
- To evaluate the role of T cells in the regulation of lymphomagenesis induced by AMuLV.
- To identify specific T cell subsets involved in resistance to AMuLV-induced lymphoma.
Main Methods:
- In vitro transformation assays using bone marrow target cells and peripheral lymph node cells.
- In vivo T cell depletion using a monoclonal antibody (mAb GK1.5) targeting L3T4+ T cells.
- Analysis of lymphoma development and characterization of lymphoma cells.
Main Results:
- Peripheral lymph node cells from naive mice inhibited in vitro AMuLV transformation of bone marrow cells.
- This inhibition was dependent on Thy-1+ L3T4+ T cells but not Lyt-2+ T cells.
- In vivo depletion of L3T4+ T cells in C57BL/6 mice led to increased susceptibility to AMuLV-induced lymphoma, with lymphoma cells expressing the P1606C3 marker.
Conclusions:
- L3T4+ T cells play a critical role in regulating lymphomagenesis induced by AMuLV.
- These T cells are essential for natural resistance to Abelson disease.
- The findings reveal a significant immunologic component in Abelson disease resistance involving L3T4+ T cells.