T-bet + B cells accumulate in adipose tissue and exacerbate metabolic disorder during obesity
Cell Metabolism, ISSN: 1550-4131, Vol: 34, Issue: 8, Page: 1121-1136.e6
2022
- 44Citations
- 73Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations44
- Citation Indexes44
- 44
- CrossRef25
- Captures73
- Readers73
- 73
Article Description
Obesity is accompanied by inflammation in adipose tissue, impaired glucose tolerance, and changes in adipose leukocyte populations. These studies of adipose tissue from humans and mice revealed that increased frequencies of T-bet + B cells in adipose tissue depend on invariant NKT cells and correlate with weight gain during obesity. Transfer of B cells enriched for T-bet + cells exacerbates metabolic disorder in obesity, while ablation of Tbx21 specifically in B cells reduces serum IgG2c levels, inflammatory cytokines, and inflammatory macrophages in adipose tissue, ameliorating metabolic symptoms. Furthermore, transfer of serum or purified IgG from HFD mice restores metabolic disease in T-bet + B cell-deficient mice, confirming T-bet + B cell-derived IgG as a key mediator of inflammation during obesity. Together, these findings reveal an important pathological role for T-bet + B cells that should inform future immunotherapy design in type 2 diabetes and other inflammatory conditions.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1550413122003011; http://dx.doi.org/10.1016/j.cmet.2022.07.002; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85135335750&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/35868310; https://linkinghub.elsevier.com/retrieve/pii/S1550413122003011; https://dx.doi.org/10.1016/j.cmet.2022.07.002
Elsevier BV
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