Lymphocytes in obesity-related adipose tissue inflammation.
Inflammation in the white adipose tissue (WAT) is considered a major player in the development of insulin resistance. The role of macrophages accumulating in the WAT during obesity, promoting WAT inflammation and insulin resistance is well established. In contrast, less is known about the role of lymphocytes. Recent studies have implicated different lymphocyte subsets in WAT inflammation. For instance, cytotoxic CD8(+) T cells infiltrating the WAT may contribute to the recruitment, differentiation and activation of macrophages. On the other hand, a differential role for CD4(+) Th1 and CD4(+) Th2 cells has been suggested. Levels of WAT regulatory T cells decrease during the course of obesity and may represent a crucial factor for the maintenance of insulin sensitivity. Moreover, activation of natural killer T cells, an innate-like T cell population, which recognises lipid antigens, promotes insulin resistance and WAT inflammation. Finally, B cells may infiltrate WAT very early in response to high-fat feeding and worsen glucose metabolism through modulation of T cells and the production of pathogenic antibodies. These interesting new findings however bear controversies and introduce novel, yet unanswered, questions. Here, we review and discuss the impact of the different lymphocyte subsets in obesity-related WAT inflammation and attempt to identify the open questions to be answered by future studies.
Department of Internal Medicine III, Division of Vascular Inflammation, Diabetes and Kidney, University Clinic Carl-Gustav-Carus, University of Dresden, Fetscherstrasse 74, 01307, Dresden, Germany. Antonios.Chatzigeorgiou@uniklinikum-dresden.de.|Institute of Physiology, University of Dresden, Dresden, Germany. Antonios.Chatzigeorgiou@uniklinikum-dresden.de.
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Chatzigeorgiou
Department of Internal Medicine III, University Clinic Carl-Gustav-Carus, University of Dresden, Dresden, Germany.|Developmental Biology Section, Biomedical Research Foundation of the Academy of Athens, Athens, Greece.|Division of Endocrinology, Children's Hospital, Boston, MA, USA.
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Karalis
Department of Internal Medicine III, University Clinic Carl-Gustav-Carus, University of Dresden, Dresden, Germany.
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Bornstein
Department of Internal Medicine III, Division of Vascular Inflammation, Diabetes and Kidney, University Clinic Carl-Gustav-Carus, University of Dresden, Fetscherstrasse 74, 01307, Dresden, Germany. Triantafyllos.Chavakis@uniklinikum-dresden.de.|Institute of Physiology, University of Dresden, Dresden, Germany. Triantafyllos.Chavakis@uniklinikum-dresden.de.
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D052436:Adipose Tissue, White / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D016175:B-Lymphocyte Subsets / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology*; D020738:Leptin / Q000502:physiology; D008214:Lymphocytes / Q000502:physiology*; D051379:Mice; D009765:Obesity / Q000473:pathology / Q000503:physiopathology*; D016176:T-Lymphocyte Subsets / Q000502:physiology
D020738:Leptin