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Related Experiment Videos

Oncogene expression in autoimmune mice.

J D Mountz1, J F Mushinski, G E Mark

  • 1Cellular Immunology Section, National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases, Bethesda, MD 20205.

The Journal of Molecular and Cellular Immunology : JMCI
|January 1, 1985
PubMed
Summary
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This study reveals that abnormal proto-oncogene expression, including MYB and MYC, is linked to the characteristic lymphocyte abnormalities seen in autoimmune diseases like lupus in mice. These findings highlight a potential molecular basis for autoimmune dysregulation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Systemic autoimmune diseases, such as systemic lupus erythematosus (SLE), are associated with abnormal lymphocyte growth and differentiation.
  • While genetic factors are implicated, the molecular mechanisms driving these cellular changes in autoimmune conditions remain incompletely understood.
  • Proto-oncogenes are known regulators of cell growth and differentiation, making them potential candidates for investigation in autoimmune pathogenesis.

Purpose of the Study:

  • To investigate the expression patterns of five key proto-oncogenes (myc, myb, abl, bas, raf) in various autoimmune mouse models.
  • To determine if aberrant proto-oncogene expression correlates with the specific lymphocyte abnormalities observed in these models.
  • To explore the molecular underpinnings of dysregulated cell growth in autoimmune disease.

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Main Methods:

  • Analysis of proto-oncogene expression (myc, myb, abl, bas, raf) in lymphoid organs and isolated cell populations from different autoimmune mouse strains (MRL-lpr/lpr, gld/gld, NZB, BXSB) and their congenic counterparts.
  • Quantitative assessment of proto-oncogene RNA levels via techniques like Northern blotting (implied by RNA measurement).
  • Cell separation methods to associate specific proto-oncogene expression with distinct lymphocyte subpopulations (T cells and B cells).

Main Results:

  • Marked, selective increase in myb expression in T cells within the lymph nodes of MRL-lpr/lpr and gld/gld mice, contrasting with subnormal levels in the thymus.
  • Elevated myc expression in the spleens of NZB and BXSB mice, associated with B cells.
  • Increased bas and abl expression linked to autoimmune B cells, with reduced expression in congenic mice carrying the xid gene.
  • Raf expression associated with both abnormal T cells and splenic B cells in MRL-lpr/lpr and gld/gld mice.

Conclusions:

  • Aberrant expression of specific proto-oncogenes is a feature of lymphocyte abnormalities in murine models of autoimmune disease.
  • The pattern of proto-oncogene dysregulation varies depending on the specific autoimmune strain and lymphocyte subset involved.
  • These findings suggest a potential role for proto-oncogenes in the molecular pathogenesis of autoimmune diseases and offer insights into lymphocyte differentiation pathways.