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Review examines the regulatory balance of T-helper and regulatory T-cell subsets in atherosclerosis, highlighting cytokine pathways that drive or dampen plaque inflammation.
Atherosclerosis is rapidly gaining recognition as an inflammatory disease showing contribution from innate and adaptive immunity pathways towards disease initiation and progression. Components of adaptive immunity especially T cells, are shown to be involved in atherogenesis and subsets of T cells are known to drive/ dampen inflammatory processes in atherosclerosis. However, the regulatory balance between the T cell subsets remains unclear. In this review, we summarize the role of T helper cells Th1, 2, 3 and 17, and regulatory cells Treg in atherosclerosis by studying the cytokines involved in Th cell functioning. We further examine the diverse roles of T helper cells for regulating the progression of atherosclerosis. Keywords: T-helper cell, atherosclerosis, cytokine, cluster of differentiation, T regulation cells, inflammatory disease, adaptive immunity, lymphocytes, leukocyte, immune system, cell-mediated immune responses, Th2 cells, humoral immune response, human atheromatous plaques, Cellular Adhesion Molecules, monocytes, macrophages, B-lymphocytes, dendritic cells, major histocompatibility complex, interferon, transforming growth factor, immunoglobulins, low-density lipoprotein receptor, apolipoprotein E, 2-glycoprotein I, rheumatoid arthritis, antiphospholipid syndrome, IFN, Natural killer T, antigen presenting cells, HMG-CoA, ApoE, P. gingivalis, CCR5, CD195, glycosaminoglycan hyaluronan, CD40, MHC II, CD80, CD86, TLR4 expression, abdominal aortic aneurysms, NF-B binding sites, oxLDL antibodies, malondialdehyde-LDL-specific, Treg cells, pro-inflammatory cytokines, Drosophila, C. pneumoniae, atherosclerotic lesions, delayed-type hypersensitivity, Inducible nitric oxide synthase, Lipopolysaccharide, Monocyte chemoattractant protein-1
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Lu et al. (2011) studied this question.
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