That the T cell profile was favorably affected in the model we used underscores an important potential link between clinical lipid management and immune function. Cholesterol, inflammatory responses and immune activation are the major components responsible for XAV939 atherosclerosis. Modulation of any of these components modifies the process of atherogenesis. Our results demonstrate that the beneficial effects of dietary lipidlowering not only affect inflammatory responses but extend into the adaptive immune system, specifically T cell responses. The report provides a new perspective on the role of cholesterol lowering in modulating the inflammatory sequelae in atherosclerosis. Sepsis has been defined as a systemic inflammatory response secondary to a proven or suspected infection. Mechanisms governing this inflammatory response have been shown to be complex and dynamic. A compensatory anti-inflammatory response also takes place during sepsis, and the balance between both responses may underlie the pathophysiology of the syndrome. Cell functional studies have underscored that the state of inflammatory response in sepsis is followed by a state of hypo-responsiveness or immunosuppression, which makes patients susceptible to late-stage infections with increased lethality. Microarray-based expression profiling is a powerful approach for the investigation of complex clinical conditions: the analysis of gene transcription at the genome level in sepsis potentially avoids results derived from biased assumptions. The application of microarray technology for biomarker discovery as well as for the comprehension of underlying mechanisms in sepsis and septic shock has been recently reviewed in the literature. Two main approaches are readily distinguishable: experimental studies including endotoxemia studies in human volunteers and sepsis in experimental animals, and microarray-based studies targeting patients with sepsis or septic shock. Despite the clear advantages of the controlled and reproducible first approach, which allows the investigator to overcome sample complexity, models are limited and cannot fully represent the inherent heterogeneity of clinical sepsis. Patient-focused studies have produced findings on the hyperactivity of pathogen recognition receptors and signaling cascade pathways in sepsis, corroborating classical paradigms in sepsis research, but have not reached consensus regarding the two-phase model of an initial hyper-inflammatory phase followed by a compensatory anti-inflammatory phase. An alternate paradigm suggests that adaptive immune dysfunction is an early feature in sepsis, as has been reported in studies addressing the gene expression profiles of peripheral blood leukocytes after endotoxin challenge in humans and mononuclear cell-specific gene expression profiles. Studies evaluating gene expression in LPS-induced tolerance models have supported a distinct scenario in which LPS-tolerant cells presenting tolerant and non-tolerant genes are driven to control inflammation, yet preserving important.