Prevalence of CD8(+)alpha beta T cells in Trypanosoma cruzi-elicited myocarditis is associated with acquisition of CD62L(Low)LFA-1(High)VLA-4(High) activation phenotype and expression of IFN-gamma-inducible adhesion and chemoattractant molecules

Citation
Pva. Dos Santos et al., Prevalence of CD8(+)alpha beta T cells in Trypanosoma cruzi-elicited myocarditis is associated with acquisition of CD62L(Low)LFA-1(High)VLA-4(High) activation phenotype and expression of IFN-gamma-inducible adhesion and chemoattractant molecules, MICROBES IN, 3(12), 2001, pp. 971-984
Citations number
60
Categorie Soggetti
Immunology
Journal title
MICROBES AND INFECTION
ISSN journal
12864579 → ACNP
Volume
3
Issue
12
Year of publication
2001
Pages
971 - 984
Database
ISI
SICI code
1286-4579(200110)3:12<971:POCBTC>2.0.ZU;2-L
Abstract
The determinants of the prevalence of CD8(+) T cells in the inflamed myocar dium of Trypanosoma cruzi-infected patients and experimental animals are un defined. Using C3H/He mice infected with the Colombiana strain of T cruzi, we found that the distribution of CD4(+)/CD8(-) and CD4(-)/CD8(+) T cells i n the myocardium mirrors the frequency of cells expressing the CD62L(Low)LF A-1(High)VLA-4(High) activation phenotype among CD4(+)/CD8(-) and CD4(-)/CD 8(+) peripheral blood T cells. Consistently, vascular cell adhesion molecul e-1-positive endothelial cells and a fine fibronectin network surrounding V LA-4(+) mononuclear cells were found in the inflamed myocardium. Further, i nterferon gamma (IFN-gamma) and IFN-gamma -induced chemokines (RANTES, MIG and CRG-2/IP-10), as well as JE/MCP-1 and MIP1-alpha, were found to be the dominant cytokines expressed in situ during acute and chronic myocarditis e licited by T cruzi. In contrast, interleukin 4 mRNA was only detected durin g the chronic phase. Altogether, the results indicate that the distribution of T-cell subsets in the myocardium of T cruzi-infected mice reflects the particular profile of adhesion molecules acquired by most peripheral CD8(+) T lymphocytes and point to the possibility that multiple IFN-gamma -induci ble molecules present in the inflamed tissue contribute to the establishmen t and maintenance of T cruzi-induced myocarditis. (C) 2001 Editions scienti fiques et medicales Elsevier SAS.