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Tissue homeostasis and cancer
Alejandro Rodríguez-Molinero1, María López-Diéguez, José R Banegas
1Department of Preventive Medicine and Public Health, Universidad Autónoma de Madrid, Arzobispo Morcillo 2, 28029, Madrid, Spain. rodriguez.molinero@gmail.com
Medical Hypotheses
|December 13, 2006
Summary
This study proposes a model for reciprocal regulation between epithelial cells and the immune system via cytokines. Dysfunctional circuits may explain links between inflammation, autoimmune diseases, and cancer development.
Area of Science:
- Immunology
- Cell Biology
- Oncology
Background:
- Epithelial cells and immune cells communicate through cytokines.
- Cytokines from epithelial cells modulate immune functions.
- Cytokines from immune cells control epithelial cell growth.
Purpose of the Study:
- To hypothesize and model the mutual regulation between epithelial cells and the immune system.
- To describe cytokine circuits involved in regulating epithelial growth and inflammation.
- To explain how dysregulation leads to disease.
Main Methods:
- Development of a theoretical model.
- Description of plausible cytokine regulatory circuits.
- Analysis of potential consequences of circuit dysfunction.
Main Results:
- A model of reciprocal growth regulation between epithelial and immune cells is proposed.
- Specific cytokine circuits are described that inhibit epithelial growth and inflammation.
- Dysfunction in these circuits is linked to neoplasia, inflammation, and autoimmune diseases.
Conclusions:
- A mutual regulatory relationship between epithelial and immune systems, mediated by cytokines, is supported.
- The model provides a framework for understanding the link between inflammation and cancer.
- Failures in immune regulation of epithelial growth can cause cancer, while failures in epithelial regulation of the immune system can cause inflammatory/autoimmune diseases.
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