Ablation of CD11c-positive cells normalizes insulin sensitivity in obese insulin resistant animals.

By D. Patsouris, Pingping Li, D. Thapar, J. Chapman, Jerrold M. Olefsky, J. Neels. Cell Metabolism, 2008

807 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/0480b452e42a6978d2ab8a455151d277a245817c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Herbert Tilg
2. G. Targher
3. A. Moschen
4. Joanne C. McNelis
5. A. Lonardo
6. A. Chawla
7. Jerrold M. Olefsky
8. Fabio Nascimbeni

In Immunology

1. J. Kirkland
2. T. Tchkonia
3. Joanne C. McNelis
4. A. Chawla
5. Jerrold M. Olefsky
6. Y. Goh
7. J. V. van Deursen
8. K. Nguyen

In Physiology

1. J. Kirkland
2. T. Tchkonia
3. Herbert Tilg
4. Joanne C. McNelis
5. A. Chawla
6. Alexander Sakers
7. T. von Zglinicki
8. S. Khosla

Citations in the corpus

• Fat Tissue, Aging, and Cellular Senescence (2010, background): “Blocking TLR4 in cells originating from bone marrow or ablating CD11c+ macrophag- es reduces insulin resistance in obese mice (Patsouris et al., 2008; Saberi et al., 2009).”
• Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “macrophages (CD11cþ cells) improves insulin sensitivity and decreases inflammation.(77) Importantly, adiponectin and PPARc promote adipose tissue macrophage polarization toward an alternative/anti-inflammatory phenotype.”
• The NALP3/NLRP3 Inflammasome Instigates Obesity-Induced Autoinflammation and Insulin Resistance (2011, background): “The activation of classically activated M1 macrophages at the expense of anti-inflammatory M2 macrophages has been causally linked to the development of adipose tissue inflammation and metabolic syndrom”
• Cellular and Molecular Players in Adipose Tissue Inflammation in the Development of Obesity-induced Insulin Resistance (2013, neutral): “However, depletion of CD11c cells by using CD11c-DTR (diphtheria toxin receptor) transgenic mice improves obesity-induced insulin resistance and decreases pro-inflammatory cytokine expression in AT and muscle [62].”
• Adipose tissue plasticity in health and disease (2022, background): “Obesity in mice and humans dramatically increases the number of adipose-tissue macrophages, linked to the activation of several inflammatory pathways (Amano et al., 2014; Patsouris et al., 2008; Weisberg et al., 2003).”
• Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, neutral): “Indeed, ablation of proinflammatory (CD11c + ) ATMs using a diphtheria toxin system led to rapid improvements in insulin sensitivity and glucose tolerance, associated with marked decreases in local and systemic inflammation in obese mice (Patsouris et al., 2008).”
• Macrophage-mediated inflammation in metabolic disease (2011, background): “Second, selective depletion of the CD11c + classically activated macrophages in CD11c-DTR mice reduces adipose tissue inflammation and improves insulin action without having a significant impact on diet-induced obesit”
• Regulatory Mechanisms for Adipose Tissue M1 and M2 Macrophages in Diet-Induced Obese Mice (2009, background): “The deletion of M1 marker genes such as TNF- (15) and C-C motif chemokine receptor (CCR) 2 (8) or the ablation of CD11c-positive cells resulted in the normalization of insulin sensitivity (16).”