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Adipose invariant NKT cells interact with CD1d-expressing macrophages to regulate obesity-related inflammation. | LitMetric

AI Article Synopsis

  • Obesity leads to chronic inflammation in adipose tissue, particularly visceral adipose tissue (VAT), which increases the risk of metabolic diseases like type 2 diabetes.
  • The study focuses on the role of CD1d-restricted natural killer T (NKT) cells in shaping the relationship between obesity and its metabolic consequences, revealing that the interaction between NKT cells and adipocytes can worsen insulin resistance.
  • Researchers found that when CD1d is specifically disrupted in macrophages (Mϕ), it unexpectedly results in increased inflammation and Aggravated production of Th1 cytokines, highlighting the complex role of CD1d in different immune cells during obesity-related inflammation.

Article Abstract

Obesity is accompanied by and accelerated with chronic inflammation in adipose tissue, especially visceral adipose tissue (VAT). This low-level inflammation predisposes the host to the development of metabolic disease, most notably type 2 diabetes. We have focused on the capacity of glycolipid-reactive, CD1d-restricted natural killer T (NKT) cells to modulate obesity and its associated metabolic sequelae. We previously reported that CD1d knockout (KO) mice are partially protected against the development of obesity-associated insulin resistance, and these findings were recapitulated in mice with an adipocyte-specific CD1d deficiency, suggesting that NKT cell-adipocyte interactions play a critical role in exacerbating disease. However, many other CD1d-expressing cells contribute to the in vivo responses of NKT cells to lipid antigens. In the present study, we examined the role of CD1d expression by macrophages (Mϕ) in the development of obesity-associated metabolic inflammation using LysMcre-cd1d1 mice where the CD1d1 gene is disrupted in a Mϕ-specific manner. Unexpectedly, these animals contained a higher frequency of T-bet CD4 T cells in VAT with increased production of Th1 cytokines that aggravated VAT inflammation. Mϕ from mutant mice displayed increased production of IL-12p40, suggesting M1 polarization. These findings indicate that interactions of CD1d on Mϕ with NKT cells play a beneficial role in obesity-associated VAT inflammation and insulin resistance with a sharp contrast to an aggravating role of CD1d in another type of antigen-presenting cell, dendritic cells.

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Source
http://dx.doi.org/10.1111/imm.13447DOI Listing

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