Interleukin-2 mastering regulation in cancer and autoimmunity

Enrique Montero, Livan Alonso, Rolando Perez, Agustin Lage

Producción científica: Capítulo del libro/informe/acta de congresoContribución a la conferenciarevisión exhaustiva

8 Citas (Scopus)


Autoimmunity and tumor immunity evolved as two distinct arenas in immunological research. However, the identification of self-antigens as the major components of malignant cells may define a central role for autoimmunity in cancer control tuned by peripheral immunoregulatory mechanisms avoiding self-aggression. Emerging evidence documents a triple antagonistic role of interleukin-2 (IL-2) in vivo promoting survival, apoptosis, and the generation of regulatory T cells. We have found that IL-2 administration reduces the clinical course of experimental autoimmune encephalomyelitis and enhances immunoregulation in tumor-bearing mice. However, actively induced anti-IL-2 antibodies restore the response to nominal antigens in tumor-induced immunosuppressed host and induced therapeutic effect in transplantable and chemically induced tumors. It is suggested that IL-2 may contribute dynamically to the maintenance of natural immunological tolerance, preventing pathological autoimmunity, but may affect antitumor immunity. Cancer research has gained from autoimmunity understanding that tumor escape strategies include the natural mechanisms of immune tolerance and the ways to imbalance the peripheral regulatory mechanisms. Interestingly, therapeutic manipulations of immunoregulation have limited antitumor effects, although promoting collaterally infrequent autoimmune diseases. It may suggest that tumors may reinforce tolerance to protect themselves from the immune attack, a process that may involve dynamically various mechanisms including IL-2. Understanding this acquired experience from tumors may help utilize them to revert the immunopathology in autoimmune diseases.

Idioma originalInglés
Título de la publicación alojadaAutoimmunity, Part C The Mosaic of Autoimmunity
EditorialBlackwell Publishing Inc.
Número de páginas12
ISBN (versión impresa)1573316628, 9781573316620
EstadoPublicada - jun. 2007
Publicado de forma externa

Serie de la publicación

NombreAnnals of the New York Academy of Sciences
ISSN (versión impresa)0077-8923
ISSN (versión digital)1749-6632


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