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Analyzing the Functions of Mast Cells In Vivo Using 'Mast Cell Knock-in' Mice
Published on: May 27, 2015
Abstract:
The recombinant (MCF) class of murine leukemia virus appears to play an important role in lymphomagenesis in AKR and other mice. Although much effort has been extended in characterizing MCF viruses, relatively little is known about the cells they infect. I examined what cells were targets in AKR mice for both lymphomagenic and nonlymphomagenic MCF viruses. Lymphomagenic MCF viruses of thymic origin (AKR-247 and C58L1) were found to infect and replicate selectively in immature lymphocytes only present in thymic cortex, whereas nonlymphomagenic MCF viruses of splenic origin (C58v-1-C77 and C58v-2-C45) selectively infected and replicated in cells that appeared to B lymphocytes. Virus-binding studies suggested that neither T- nor B-lymphocyte tropisms were determined by selective attachment of virus to the respective cells. These findings demonstrate that in contrast with ecotropic viruses, which can infect many types of cells in the mouse, specific cellular tropisms can exist for MCF viruses, and that MCF infection, and therefore oncogenicity, is closely linked to cellular differentiation.
Insights
Murine leukemia viruses (MCF) cause lymphoma by infecting specific immature lymphocytes. Lymphomagenic MCF viruses target thymic cortex lymphocytes, while non-lymphomagenic MCF viruses target B lymphocytes, revealing a link between MCF infection and cellular differentiation.
Area of Science:
- Virology
- Immunology
- Oncology
Background:
- Murine leukemia viruses (MCF) are implicated in mouse lymphomagenesis.
- Understanding the cellular targets of MCF viruses is crucial for comprehending their oncogenic potential.
- Limited information exists regarding the specific cell types infected by different MCF virus strains.
Purpose of the Study:
- To identify the target cells of both lymphomagenic and non-lymphomagenic MCF viruses in AKR mice.
- To investigate the relationship between MCF virus tropism and cellular differentiation.
- To explore the mechanisms underlying MCF virus cellular tropism.
Main Methods:
- Infection studies using lymphomagenic (AKR-247, C58L1) and non-lymphomagenic (C58v-1-C77, C58v-2-C45) MCF viruses in AKR mice.
- Analysis of viral replication in different lymphocyte populations within the thymus and spleen.
- Virus-binding assays to assess the role of cell surface attachment in determining tropism.
Main Results:
- Lymphomagenic MCF viruses selectively infected and replicated in immature lymphocytes of the thymic cortex.
- Nonlymphomagenic MCF viruses selectively infected and replicated in cells identified as B lymphocytes.
- Virus-binding studies indicated that selective attachment to T or B lymphocytes does not determine MCF virus tropism.
Conclusions:
- MCF viruses exhibit specific cellular tropisms, unlike ecotropic viruses.
- MCF virus infection and subsequent oncogenicity are closely associated with the differentiation state of the target cell.
- These findings highlight the importance of cellular differentiation in dictating MCF virus tropism and lymphomagenic potential.

