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
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
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.