Abstract
TIM-3 as a molecular switch for tumor escape from innate immunity
Highlights
Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interaction between the receptor TIM-3 and the alarmin HMGB1 by Chiba et al (2012)
Chiba and coworkers have evidenced the existence of a comprehensive mechanistic pathway by which the tumor microenvironment affects dendritic cell ability to regulate nucleic acid-mediated innate immune pathways through TIM-3
Immunosuppressive factors, such as VEGF-A and IL-10 released by tumor cells, induce expression of TIM-3 in dendritic cells which results in impaired response to nucleic acid-stimulated tumor immunity
Summary
Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interaction between the receptor TIM-3 and the alarmin HMGB1 by Chiba et al (2012). Chiba and coworkers have evidenced the existence of a comprehensive mechanistic pathway by which the tumor microenvironment affects dendritic cell ability to regulate nucleic acid-mediated innate immune pathways through TIM-3. Immunosuppressive factors, such as VEGF-A and IL-10 released by tumor cells, induce expression of TIM-3 in dendritic cells which results in impaired response to nucleic acid-stimulated tumor immunity.
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