Adaptive immunity in atherosclerosis: mechanisms and future therapeutic targets

Nat Rev Cardiol. 2011 Jun;8(6):348-58. doi: 10.1038/nrcardio.2011.62. Epub 2011 Apr 19.

Abstract

Chronic inflammation drives the development of atherosclerosis, and adaptive immunity is deeply involved in this process. Initial studies attributed a pathogenic role to T cells in atherosclerosis, mainly owing to the proatherogenic role of the T-helper (T(H))-1 cell subset, whereas the influence of T(H)2 and T(H)17 subsets is still debated. Today we know that T regulatory cells play a critical role in the protection against atherosclerotic lesion development and inflammation. In contrast to T cells, B cells were initially considered to be protective in atherosclerosis, assumingly through the production of protective antibodies against oxidized LDL. This concept has now been refined and proatherogenic roles of certain mature B cell subsets have been identified. We review the current knowledge about the role of various lymphocyte subsets in the development and progression of atherosclerosis and highlight future targets for immunomodulatory therapy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptive Immunity* / drug effects
  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Atherosclerosis / drug therapy
  • Atherosclerosis / immunology*
  • B-Lymphocyte Subsets / drug effects
  • B-Lymphocyte Subsets / immunology*
  • Humans
  • Immunologic Factors / therapeutic use
  • Inflammation / drug therapy
  • Inflammation / immunology*
  • Inflammation Mediators / metabolism
  • T-Lymphocyte Subsets / drug effects
  • T-Lymphocyte Subsets / immunology*
  • Vaccines

Substances

  • Anti-Inflammatory Agents
  • Immunologic Factors
  • Inflammation Mediators
  • Vaccines