The article was published on Nature Immunology in May 2019. The authors Hatoon Baazim et al (CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria) describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8+ T cells in IAC.
Background & Aims & Conclusions
Cachexia is a major cause of morbidity and mortality for various cancers, chronic inflammation, and infections. Although several treatment options have been explored, such as ghrelin agonists, the standard of care to prevent or reduce cachexia remains unclear.
In this study, the authors used the chronic viral infection mice model to elucidate the inflammatory drivers of IAC.
The researchers designed a comprehensive approach based on genetic, dietary, and pharmacological interventions to reveal the common and unique characteristics of the CAC and IAC.
The results showed that cytokines linked to cancer-associated cachexia did not contribute to IAC. In contrast, virus-specific CD8+ T cells induce morphological and molecular changes in adipose tissue that result in depletion of lipid storage. These changes required T cell–intrinsic type I interferon signaling and antigen-specific priming. These results link the systemic antiviral immune response with adipose tissue remodeling, revealing the important role of CD8+ T cells in IAC.
This study helps us to understand the mechanisms that cause cachexia in different inflammatory and disease Settings.
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The free thyroxine levels of both infected and uninfected mice were measured by ELISA kit from CUSABIO according to manufacturer’s instructions.
