This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hansson, G. K. Search for Related Content PubMed PubMed Citation Articles by Hansson, G. K. Related Collections Cardiovascular imaging agents/Techniques Acute coronary syndromes CV surgery: aortic and vascular disease

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:523.)
© 2002 American Heart Association, Inc.

Editorials

The B Cell

A Good Guy in Vascular Disease?

Göran K. Hansson

From the Center for Molecular Medicine, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.

Correspondence to Göran K. Hansson, Center for Molecular Medicine, Karolinska Institute, Building 8:03, Karolinska Hospital, SE-17176 Stockholm, Sweden. E-mail Goran.Hansson@cmm.ki.se

Inflammatory cells and molecules have largely been considered bad guys in the pathogenesis of atherosclerosis and other vascular diseases. This is particularly true for macrophages, T cells, and mast cells. In contrast, the role of B cells has remained unclear.¹ Recent studies suggest that this cell type may inhibit the development of vascular pathology in models of atherosclerosis and restenosis.^2,3 The Table summarizes some experiments addressing the effect on atherosclerosis of cells involved in adaptive immunity.

View this table: [in this window] [in a new window]   Table 1. Effect of Immune Defects and Immune Cell Transfer on Lesion Development in Vascular Disease Models

See page 644

The case for the monocyte-derived macrophage is particularly strong. It can oxidize lipoproteins, express scavenger receptors, and accumulate cholesteryl esters. It is also capable of producing tissue factor, and it is a major source of matrix metalloproteinases and proinflammatory cytokines. All of these factors and phenomena are considered proatherogenic. Direct support for the conclusion that macrophages promote atherosclerosis was obtained in studies of mice deficient in functional macrophage-colony stimulating factor.⁴ When such mice were crossed with atherosclerosis-prone apolipoprotein E–deficient (apoE-/-) mice, the offspring developed little, if any, atherosclerosis. This implies that monocyte differentiation into macrophages is a necessary step in the development of atherosclerosis.

T cells as well as B cells can respond to athero-antigens such as oxidized LDL and heat shock proteins. The predominant T cell subtype in atherosclerotic lesions, the CD4+ Th1 cell, responds to antigenic challenge by releasing proinflammatory cytokines including interferon-, tumor necrosis factor– and lymphotoxin.¹ ApoE-/- mice that lack adaptive . . . [Full Text of this Article]

This article has been cited by other articles:

				N. Li Platelet-lymphocyte cross-talk J. Leukoc. Biol., May 1, 2008; 83(5): 1069 - 1078. [Abstract] [Full Text] [PDF]

				M. Madjid, R. V. Luepker, K. J. Greenlund, K. A. Taubert, M. J. Roy, and R. M. Robertson Task Force IV: Cardiovascular Effects of Emerging Infectious Diseases and Biological Terrorism Threats: Basic, Clinical, and Population Science Research and Training Needs J. Am. Coll. Cardiol., March 27, 2007; 49(12): 1407 - 1412. [Full Text] [PDF]

				M. P.W. Moos, N. John, R. Grabner, S. Nossmann, B. Gunther, R. Vollandt, C. D. Funk, B. Kaiser, and A. J.R. Habenicht The Lamina Adventitia Is the Major Site of Immune Cell Accumulation in Standard Chow-Fed Apolipoprotein E-Deficient Mice Arterioscler Thromb Vasc Biol, November 1, 2005; 25(11): 2386 - 2391. [Abstract] [Full Text] [PDF]

				A. Coppola, L. Coppola, L. dalla Mora, F. M. Limongelli, A. Grassia, L. Mastrolorenzo, G. Gombos, and G. Lucivero Vigorous exercise acutely changes platelet and B-lymphocyte CD39 expression J Appl Physiol, April 1, 2005; 98(4): 1414 - 1419. [Abstract] [Full Text] [PDF]

				A. P. Burke, R. Virmani, Z. Galis, C. C. Haudenschild, and J. E. Muller Task force #2--what is the pathologic basis for new atherosclerosis imaging techniques? J. Am. Coll. Cardiol., June 4, 2003; 41(11): 1874 - 1886. [Full Text] [PDF]