Adaptive immunity in atherogenesis: new insights and therapeutic approaches
Andrew H. Lichtman, … , Sotirios Tsimikas, Joseph L. Witztum
Andrew H. Lichtman, … , Sotirios Tsimikas, Joseph L. Witztum
Published January 2, 2013
Citation Information: J Clin Invest. 2013;123(1):27-36. https://doi.org/10.1172/JCI63108.
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Adaptive immunity in atherogenesis: new insights and therapeutic approaches

Abstract

Many remarkable advances have improved our understanding of the cellular and molecular events in the pathogenesis of atherosclerosis. Chief among these is the accumulating knowledge of how the immune system contributes to all phases of atherogenesis, including well-known inflammatory reactions consequent to intimal trapping and oxidation of LDL. Advances in our understanding of the innate and adaptive responses to these events have helped to clarify the role of inflammation in atherogenesis and suggested new diagnostic modalities and novel therapeutic targets. Here we focus on recent advances in understanding how adaptive immunity affects atherogenesis.

Authors

Andrew H. Lichtman, Christoph J. Binder, Sotirios Tsimikas, Joseph L. Witztum

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Figure 2

Costimulatory and coinhibitory molecules and their receptors.

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Costimulatory and coinhibitory molecules and their receptors. Costimulat...
Costimulatory molecules, expressed on APCs, engage receptors on T cells concurrent with antigen recognition and induce signals that are required for naive T cell activation or that enhance effector/memory T cell responses. Coinhibitory receptors (CTLA-4 and PD-1) are expressed on activated T cells and, upon binding ligands on APCs, inhibit T cell responses. The major costimulatory and coinhibitory molecules, which belong to the B7/CD28 families or TNF/TNFR superfamilies, are shown in the table.