A Dual Role of CD4 + T Cells in Adipose Tissue?

Abstract

See related articles, pages 961–968 Recent studies project an exponential increase in type 2 diabetes mellitus, obesity, and the metabolic syndrome not only in Western but also in developing countries.1 This perspective suggests an alarming rise in morbidity, mortality, and health care costs associated with these diseases. Thus, for improving prevention, diagnosis, and therapy of these diseases, we need a better understanding of the genetic, molecular, cellular, and environmental interactions that govern these metabolic derangements. Chronic inflammation plays a pivotal role in insulin resistance and obesity that shares many pathogenetic aspects with atherogenesis.2 Hotamisligil and coworkers were the first to describe a role of proinflammatory cytokines in obesity. They reported an increase in tumor necrosis factor (TNF)α in the white adipose tissue of obese mice that correlated with insulin resistance.3 Meanwhile, this notion has been extended from mice to men and to other cytokines such as monocyte chemoattractant protein (MCP)-1, interleukin (IL)-1, and IL-6 that have been found to be involved in obesity and insulin resistance.4–6 At the cellular level, most reports have highlighted macrophages as the key directors of this inflammatory concert.5,6 Less is known about the role of adaptive immunity in obesity. Recent studies reveal that obese mice and men also exhibit an increase in adipose tissue T cells and the corresponding chemokines such as RANTES (regulated on activation, normal T-cell expressed and secreted) or cytokines such as interferon (IFN)-γ.7,8 Nevertheless, the relevance of T cells in this context remains to be determined.9 …