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Infection and Immunity, November 1999, p. 6177-6180, Vol. 67, No. 11
Departments of
Immunology1 and General
Microbiology,3 Instituto de
Microbiologia Prof. Paulo de Góes and Instituto de
Biofísica Carlos Chagas Filho,2
Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil, and
Division of Immunology, Department of Medicine, Uniformed
Services University of the Health Sciences, Bethesda,
Maryland4
Received 26 March 1999/Returned for modification 29 April
1999/Accepted 24 August 1999
Glycoinositolphospholipids (GIPLs) are some of the major
glycolipids of the Trypanosoma cruzi surface that were
previously shown to activate B cells. In the present study, we
investigated whether (i) T. cruzi GIPLs could induce
immunoglobulin secretion from B cells in the absence of T cells and NK
cells and whether (ii) NK cells are also stimulated by the GIPLs. B
cells purified from mice deficient in both T and NK cells (CD3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Modulation of B-Lymphocyte and NK Cell Activities
by Glycoinositolphospholipid Purified from Trypanosoma
cruzi
transgenic mice) secreted immunoglobulin in response to the GIPL. This
response was increased by coculture with a murine NK cell line. The
T. cruzi GIPL also increased the NK cell (interleukin-2
induced) proliferative response. Our data indicate that the T. cruzi GIPL has a direct stimulatory effect on NK cells and
induces immunoglobulin secretion in the absence of T lymphocytes and NK
cells. These findings suggest that this T. cruzi-derived
molecule may be one of the stimulators that lead to NK cell activation
during T. cruzi infection.
*
Corresponding author. Mailing address: Departamento de
Imunologia, Instituto de Microbiologia Prof. Paulo de Góes, CCS,
Bloco I, Universidade Federal do Rio de Janeiro, Cidade
Universitária, Ilha do Fundao, 21941-970 Rio de Janeiro, RJ,
Brazil. Phone and fax: (55-21) 560-8344. E-mail:
imimlgl{at}microbio.ufrj.br.
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