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Published on: April 21, 2015
Cytokine and T-cell subset abnormalities in immunodeficient wasted mice
C R Libertin1, L Ling-Indeck, M Padilla
1Department of Pathology, Loyola University Medical Center, Maywood, IL 60153.
Molecular Immunology
|July 1, 1994
Summary
The wasted mouse mutation (wst/wst) causes immunodeficiency and faulty DNA repair. Cytokine gene expression is imbalanced, with reduced IL5 and increased IL2, gamma-interferon, and beta-TGF, suggesting a role in the observed abnormalities.
Area of Science:
- Immunology
- Genetics
- Molecular Biology
Background:
- The autosomal recessive mutation (wst/wst) in wasted mice leads to neurological issues, immune deficiency, and DNA repair defects.
- Immunodeficiency in these mice includes reduced thymus-to-body weight ratio, low IgA plasma cells, and increased T-cell sensitivity to radiation.
Purpose of the Study:
- To investigate T-cell activity and cytokine gene expression in wasted mice to understand the underlying mechanisms of their abnormalities.
Main Methods:
- Flow cytometry was used to analyze T-cell subpopulations (CD4+, CD8+).
- Gene expression of various cytokines (IL1, IL2, IL2R, TNF, IL5, gamma-interferon, beta-TGF) was examined in lymphoid tissues using dot blot and Northern blot hybridizations.
Main Results:
- Wasted mice exhibited normal percentages of thymic and splenic Thy1+, CD4+, and CD8+ cells, but with altered CD4/CD8 co-expression.
- Significant alterations in cytokine mRNA levels were observed: decreased IL5 and IL2 receptor (IL2R) expression, increased IL1, IL2, gamma-interferon, and beta-transforming growth factor (beta-TGF) expression.
- Tumor necrosis factor (TNF) mRNA expression remained unaffected.
Conclusions:
- The study suggests that a cytokine imbalance, characterized by specific deficiencies and excesses in gene expression, plays a critical role in the pathogenesis of the immunodeficiency and other abnormalities seen in wasted mice.
