Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Immune System Disorder and Cancer-Associated Cachexia

Version 1 : Received: 10 April 2024 / Approved: 11 April 2024 / Online: 11 April 2024 (11:24:37 CEST)

A peer-reviewed article of this Preprint also exists.

Zhang, L.; Bonomi, P.D. Immune System Disorder and Cancer-Associated Cachexia. Cancers 2024, 16, 1709. Zhang, L.; Bonomi, P.D. Immune System Disorder and Cancer-Associated Cachexia. Cancers 2024, 16, 1709.

Abstract

Cancer-associated cachexia (CAC) is a debilitating condition marked by muscle and fat loss, unresponsive to nutritional support, and contributes significantly to morbidity and mortality in patients with cancer. Immune dysfunction, driven by cytokine imbalance, contributes to CAC progression. This review explores the potential relationship between CAC and anti-cancer immune response in pre-clinical and clinical studies. Pre-clinical studies showcase the involvement of cytokines like IL-1β, IL-6, IL-8, IFN-γ, TNF-α, and TGF-β, in CAC. IL-6 and TNF-α, interacting with muscle and adipose tissues, induce wasting through JAK/STAT and NF-κB pathways. Myeloid-derived suppressor cells (MDSCs) exacerbate CAC by promoting inflammation. Clinical studies confirm elevated pro-inflammatory cytokines (IL-6, IL-8, TNFα) and immune markers like neutrophil-to-lymphocyte ratio (NLR) in patients with CAC. Thus, immunomodulatory mechanisms involved in CAC may impact the anti-neoplastic immune response. Inhibiting CAC mechanisms could enhance anti-cancer therapies, notably immunotherapy. R-ketorolac, a new immunomodulator, reversed weight loss and increased survival in mice. Combining these agents with immunotherapy may benefit patients with cancer experiencing CAC. Further research is vital to understand the complex interplay between tumor-induced immune dysregulation and CAC during immunotherapy.

Keywords

CAC; cytokines; immune disorder; inflammation; muscle wasting; IL-6; TNF-α

Subject

Biology and Life Sciences, Life Sciences

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.

Leave a public comment
Send a private comment to the author(s)
* All users must log in before leaving a comment
Views 0
Downloads 0
Comments 0
Metrics 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.
We use cookies on our website to ensure you get the best experience.
Read more about our cookies here.