| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
71-180 |
DRI_Challenge |
denotes |
epresents a leading cause of morbidity and mortality in various cancers, chronic inflammation and infections. |
| T2 |
181-306 |
DRI_Background |
denotes |
Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-associated cachexia (IAC). |
| T3 |
307-463 |
DRI_Challenge |
denotes |
In the present paper we describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8+ T cells in IAC. |
| T4 |
464-537 |
DRI_Background |
denotes |
Cytokines linked to cancer-associated cachexia did not contribute to IAC. |
| T5 |
538-546 |
DRI_Background |
denotes |
Instead, |
| T6 |
567-678 |
DRI_Background |
denotes |
T cells caused morphologic and molecular changes in the adipose tissue, which led to depletion of lipid stores. |
| T7 |
679-856 |
DRI_Approach |
denotes |
These changes occurred at a time point that preceded the peak of the CD8+ T cell response and required T cell-intrinsic type I interferon signaling and antigen-specific priming. |
| T8 |
857-998 |
DRI_Outcome |
denotes |
Our results link systemic antiviral immune responses to adipose-tissue remodeling and reveal an underappreciated role of CD8+ T cells in IAC. |
