Experimental infection with Trypanosoma cruzi increases the population of CD8(+), but not CD4(+), immunoglobulin G Fc receptor-positive T lymphocytes.

Abstract:

:It is well established that activating-type Fc receptors for immunoglobulin G (FcgammaR), such as FcgammaRI and FcgammaRIII, are essential for inducing inflammatory responses. On the other hand, a unique inhibitory FcgammaR, FcgammaRIIB, inhibits intracellular signaling upon engagement of immunoglobulin G-immune complexes, suppressing inflammation and autoimmunity. The expression of FcgammaRIIB on B lymphocytes, natural killer cells, macrophages, mast cells, and a number of other cell types has been demonstrated for many years. However, the expression on T lymphocytes is probably restricted to activated cells in a narrow window of time. The controversy regarding the FcgammaR expression on T lymphocytes is attributable to considerable heterogeneity of cellular subpopulations and activation stages during immune responses in vivo. We addressed here this question by using mice experimentally infected with Trypanosoma cruzi, and we found an increase in the CD8(+) FcgammaR(+) population but not in the CD4(+) FcgammaR(+) population. Moreover, CD8(+) FcgammaR(+) T cells predominantly composed the cardiac inflammatory infiltration induced by the infection. These results indicate a novel pattern of FcgammaR expression on T cells in a pathological situation, and possible functional roles of this phenomenon are discussed.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

Henriques-Pons A,Olivieri BP,Oliveira GM,Daëron M,de Araújo-Jorge TC

doi

10.1128/IAI.73.8.5048-5052.2005

keywords:

subject

Has Abstract

pub_date

2005-08-01 00:00:00

pages

5048-52

issue

8

eissn

0019-9567

issn

1098-5522

pii

73/8/5048

journal_volume

73

pub_type

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