'Galectin-1 Induces Central and Peripheral Cell Death: Implications in T-Cell Physiopathology'
| Autor: | G. A. Rabinovich, C. E. Sotomayor |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Programmed cell death
Galectin 1 Galectin 3 T-Lymphocytes T cell Immunology Biology immunomodulation Immune tolerance Immune system Immune privilege Cell Adhesion Immune Tolerance medicine Animals Homeostasis Humans galectin-1 fas Receptor autoimmunity apoptosis Antigens Differentiation macrophages Cell biology Hemagglutinins medicine.anatomical_structure Galectin-3 Apoptosis Galectin-1 Research Article Developmental Biology |
| Zdroj: | Developmental Immunology |
| ISSN: | 1044-6672 |
| DOI: | 10.1155/2000/36321 |
| Popis: | The immune system has a remarkable capacity to maintain a state of equilibrium even as it responds to a diverse array of foreign proteins and despite its contact exposure to self-antigens. Apoptosis is one of the mechanisms aimed at preserving the homeostasis after the completion of an immune response, thus returning the immune system to a basal state and warranting the elimination of autoagressive cells in both central and peripheral lymphoid organs. Targeted deletions in critical genes involved in the apoptotic death machinery together with natural spontaneous mutations have clearly shown the importance of apoptosis in the regulation of the immune response. This complex scenario of stimulatory and inhibitory genes has been enriched with the finding that galectin-1, a 14.5 kDa β-galactoside-binding protein, is able to induce apoptosis of immature cortical thymocytes and mature T cells by cross-linking cell surface glycoconjugates. Galectin-1 is present not only in central and peripheral lymphoid organs, but also at sites of immune privilege. In the present article we will discuss the implications of galectin-1-induced apoptosis in T-cell physiopathology in an attempt to validate its therapeutic potential in autoimmune and inflammatory diseases. |
| Databáze: | OpenAIRE |
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