Why we lose fat and muscle during infection explained in new research

New Delhi: T cells, or body cells involved in immune responses, are responsible for causing fat and muscle loss during infection, new research in mice has revealed.

Fat and muscle loss, a process called wasting, were brought about by different groups of immune cells, researchers from the Salk Institute for Biological Studies, California, US, found.

Further, they found, while muscle loss helped the mice fight and survive infection, fat loss had no impact on the mice's ability to fight or survive infection.

While wasting is known to coincide with higher mortality rates, wasting may help manage illness, according to the researchers.

The findings, published in the journal Cell Reports, help understand how wasting influences survival and morbidity across infections, cancers, chronic illnesses, and more and could better inform therapeutic interventions to avoid wasting in patients.

For the study, the researchers were interested in examining the activity of CD4+ and CD8+ T cells. CD4+ T cells lead the fight against infection and promote the activity of CD8+ T cells, which kill invaders and cancerous cells.

Given that these groups of T cells often work together, their combined activity was hypothesised to contribute to wasting.

The researchers infected the mice with the parasite T. brucei, known to live in fat and be capable of blocking adaptive immune response cells, including T cells, so as to understand how T cells mediate fat loss.

They found that acting first, CD4+ T cells initiated the process of fat wasting. This was followed by, yet independent of fat wasting, CD8+ T cells initiating muscle wasting.

They then found that fat wasting, induced by CD4+ T cells, had no impact on the mice's ability to fight the T. brucei infection. However, CD8+ T cell-induced muscle wasting was found to help the mice fight T. brucei and survive the infection.

"Our discoveries were so surprising that there were times I wondered if we did something wrong," said first author Samuel Redford, a current visiting researcher at the institute.

"We had striking results that mice with fully functioning immune systems and mice without CD4+ T cells lived the same amount of time - meaning, those CD4+ T cells and the fat wasting they caused were completely disposable in fighting the parasite. And beyond that, we found that normally cooperative T cell subtypes were working totally independently of one another." The team in future intends to study T cell mechanisms in other mammals and, eventually, in humans.