Differential expression of adhesion moleculesshaping the T-cell subset prevalence during the early phase of autoimmune and Trypanosoma cruzi-elicited myocarditis

Abstract

The participation of cell adhesion molecules (CAMs)

Intercellular Adhesion Molecule 1 Deficiency Leads to Impaired Recruitment of T Lymphocytes and Enhanced Host Susceptibility to Infection withTrypanosoma cruzi

“…Moreover, ICAM-1 ϩ and VCAM-1 ϩ blood vessels were associated with the presence of CD8 ϩ -infiltrating T cells in the cardiac tissue of chagasic patients with severe cardiomyopathy (38). In addition, cardiomyocytes express ICAM-1 during the acute phase of experimental T. cruzi infection (27,30). Considering that ICAM-1-mediated interactions plays a crucial role in forming the immunological synapse (29,39), ICAM-1 ϩ myocytes could be targets for LFA-1 ϩ cytotoxic T cells, contributing to heart dysfunction during chagasic myocarditis.…”

“…Furthermore, the induction and up-regulation of expression of VCAM-1, a VLA-4 ligand (28), and ICAM-1, a LFA-1 ligand (28), on cardiac vascular endothelium were associated with the establishment of the early acute T. cruzi-elicited myocarditis (27). Moreover, ICAM-1 ϩ and VCAM-1 ϩ blood vessels were associated with the presence of CD8 ϩ -infiltrating T cells in the cardiac tissue of chagasic patients with severe cardiomyopathy (38).…”

“…This proinflammatory activity of IFN-␥ is associated with its ability to promote the local production of certain chemokines, such as CCL5/RANTES, CXCL9/monokine induced by IFN-␥ (MIG), and CXCL10/IFN-␣-inducible protein 10 (IP-10), which are important in mediating the migration of activated CD4 ϩ and CD8 ϩ ␣␤ T lymphocytes (5,13,14,25). In T. cruzi-infected animals, expression of cellular adhesion molecules (CAMs) such as ICAM-1 and VCAM-1 is induced in the cardiac tissue, whereas a high percentage of peripheral blood T lymphocytes become highly positive for LFA-1, ICAM-1, and VLA-4 during the early acute and chronic phase (14,26,27). However, the crucial elements controlling the expression of these CAMs and their importance in cell recruitment and host resistance to infection have been poorly investigated.…”

Interferon-γ and other inflammatory mediators in cardiomyocyte signaling during Chagas disease cardiomyopathy

“…The blockade of one, CCR5, by Met-RANTES significantly decreased the intensity of cardiac inflammatory infiltrate, suggesting that lymphocyte migration to the myocardium during acute infection is dependent on CCR5 ligands [42,43] . IFN-γ-inducible adhesion molecules, such as fibronectin and VCAM-1, can also be detected at high levels in cardiac tissue from T. cruzi-infected mice [44] . Few studies have investigated the immunology of the acute phase infection in human patients.…”

CC-chemokine receptors: a potential therapeutic target for Trypanosoma cruzi-elicited myocarditis

“…Studying C3H/He mice chronically infected with the Colombiana strain of T. cruzi we showed the prevalence of CD8 + T cells in the inflamed heart (dos Santos et al 2001). Further, recently we have shown that the establishment of the CD8 + T cells predominance in the cardiac tissue of T. cruziinfected mice is a rather precocious process, being detected during the early acute phase (Marino et al 2003a). Trying to understand the molecular mechanisms involved in T. cruzi-elicited myocarditis with prevalence of CD8 + T cells, we have investigated the expression of inflammatory CC-chemokines in the heart of Colombiana straininfected C3H/He mice.…”