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Frontiers in Cell and Developmental Biology

Mice lacking a liver protein develop chronic inflammation

In experiments with genetically altered mice, overactive immune cells alone did not reproduce the widespread inflammation seen in old animals lacking the protein.

Paper by Huiying Sun, Miao Yu, Ran Xu et al.

Liver tissue crowded with immune cells sits beside a mouse with skin lesions, contrasted with less crowded tissue and a mouse with intact skin.
Accepted, not yet published: experiments in Fgl1 knockout miceMechanisms

Limit: T cell contributions alongside other inflammatory factors were not measured

Edited by Boris Djordjevic · AgingResearch.News

Paper
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Mice genetically engineered to lack FGL1, a liver-secreted protein, developed chronic inflammation throughout the body as they aged in animal experiments. Signs appeared only in aged animals. They included skin lesions, immune cells entering multiple organs and higher blood levels of inflammation-promoting proteins.

Before inflammation began, adult and middle-aged mice had normal development of T and B cells, two types of immune cells. Their T cells also responded normally to stimulation of their receptors, which detect signals that activate them. Aged mice lacking the protein had overactive T cells. But transferring those cells into recipient mice with unusually few lymphocytes—a group of immune cells—did not reproduce the systemic inflammation. The findings suggested that T cell overactivity was not the primary driver of the condition.

Why it matters

The work addresses how the body keeps immune activity in check with age, and what might account for chronic inflammation that emerges late in life.

Caveats

The transfer experiment tested whether T cells alone could reproduce inflammation, not whether they contributed alongside other factors. The findings came from genetically modified mice, not people.

Where the evidence stands

Adoptive t cell transfer

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

  • 1 lab

Inflammation

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

No results posted: trials that ended over a year ago with no results on ClinicalTrials.gov and no paper reporting them.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

Includes the processes named after it and trials of drugs aimed at it.

  • 986 independent labs in 73 countries
  • 188 findings against
  • 1,913 trials, 540 with no results posted
  • Funders: National Institutes of Health and others
  • 361 of 4,268 findings with company ties
  • 1,455 of 1,913 trials sponsored by developers of drugs on it

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The paper

T cell hyperactivation is not the primary driver of age-associated systemic inflammation induced by FGL1 deficiency

Huiying Sun, Miao Yu, Ran Xu et al.

Frontiers in Cell and Developmental Biology, Oct 30, 2026, CC BY, Accepted, not yet published

Journal site

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