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Infection and Immunity, August 2005, p. 5048-5052, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.5048-5052.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Experimental Infection with Trypanosoma cruzi Increases the Population of CD8⁺, but not CD4⁺, Immunoglobulin G Fc Receptor-Positive T Lymphocytes

Laboratorio Biologia Celular-DUBC-Instituto Oswaldo Cruz FIOCRUZ, Rio de Janeiro, Brazil,¹ Unité d'Allergologie Moléculaire et Cellulaire, Département d'Immunologie, Institut Pasteur, Paris, France²

Received 28 August 2003/ Returned for modification 20 December 2004/ Accepted 14 March 2005

It is well established that activating-type Fc receptors for immunoglobulin G (FcR), such as FcRI and FcRIII, are essential for inducing inflammatory responses. On the other hand, a unique inhibitory FcR, FcRIIB, inhibits intracellular signaling upon engagement of immunoglobulin G-immune complexes, suppressing inflammation and autoimmunity. The expression of FcRIIB 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 FcR 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⁺ FcR⁺ population but not in the CD4⁺ FcR⁺ population. Moreover, CD8⁺ FcR⁺ T cells predominantly composed the cardiac inflammatory infiltration induced by the infection. These results indicate a novel pattern of FcR expression on T cells in a pathological situation, and possible functional roles of this phenomenon are discussed.

Editor: J. F. Urban, Jr.