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Phenotypic characterization of Innate Lymphoidal Cells in coronary heart disease patients
Dr. Max Wacker, Prof. Dr. med. Jens Wippermann
The global scenario of diseases is shifting from communicable to non-communicable diseases (NCDs), which kill about 41 million people each year. This accounts for 71% of all deaths in the world and therefore NCDs are gaining importance in the health care sectors. Among them, cardiovascular diseases (CVDs) are the first leading cause of death, according to the estimates by the World Health Organization (WHO), where 17.9 million people die of CVDs each year that already accounts for 31.3% of the total death worldwide. Given the fact that the deposition of low density lipoprotein (LDL) in the arterial intima is responsible for initiating atherosclerotic lesions, the deposited lipid induced inflammation is well proven to be the major contributing factor for the progression and sustainment of atherosclerosis in patients with coronary heart disease . Here, both innate and adaptive cells are known to be the key components for the formation of atherosclerotic lesion, where macrophages and CD4+ T cells are the critical players . In contrast, Group 2 innate lymphoid cells (ILC2s), which emerge into a separate cell lineage distinct from the natural killers (NK) cells , were implicated in limiting the obesity by accumulating beige adipocytes . Since obesity is a major confounding factor for the development of CHD, an alteration in lipid metabolism by reducing the LDL levels underscores the atheroprotective potential of ILC2s and thereby directly evidenced for their cardio-protective effects in reducing atherogenesis and plaque size and composition in atherosclerosis mouse model [9, 10]. The ILC2s are found in tissues as well as in circulating blood . However, until now, there is no report demonstrating the role of ILC2s in the patients with CHD. The overall aim of the proposed study is to gain desirable and adequate knowledge on characterization of ABA and its receptors and immune-phenotyping of ILC2s between CHD patients and normal controls
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