Down-regulation of human B lymphocyte activities by a Trypanosoma cruzi membrane glycoprotein

Citation
F. Kierszenbaum et Mb. Sztein, Down-regulation of human B lymphocyte activities by a Trypanosoma cruzi membrane glycoprotein, INT J PARAS, 31(3), 2001, pp. 265-271
Citations number
30
Categorie Soggetti
Biology,Microbiology
Journal title
INTERNATIONAL JOURNAL FOR PARASITOLOGY
ISSN journal
00207519 → ACNP
Volume
31
Issue
3
Year of publication
2001
Pages
265 - 271
Database
ISI
SICI code
0020-7519(200103)31:3<265:DOHBLA>2.0.ZU;2-9
Abstract
The effects of purified AGC10, a Trypanosoma cruzi membrane glycoprotein, o n normal human B lymphocytes were studied in this work. In the presence of AGC10, [H-3]-thymidine uptake by human peripheral blood mononuclear cells s timulated with the B cell-specific mitogen SACI (killed Staphylococcus aure us Cowan I) was markedly decreased. This alteration was accompanied by othe rs such as decreased expression of the CD122 and CD132 chains of the IL-2R complex. These inhibitory effects appeared to be somewhat selective, as exp ression of CD25, another IL-2R chain, was not affected by AGC10 and no sign ificant modification occurred in the expression of the B-cell-specific mark er CD19 or CD21. In contrast, AGC10 did reduce the levels of expression of CD86 and CD80, molecules known to play critical roles in B cell interaction s with T lymphocytes. Fairly large subpopulations of, but not all, B lympho cytes had their expression of CD122(+), CD132(+), CD86(+) and CD80(+) reduc ed to undetectable levels in the presence of AGC10. However, the SACI-activ ated B cells that remained capable of expressing these molecules in the pre sence of AGC10 did so at normal levels. This was denoted by comparable mean fluorescence intensity values representing the expression of CD122, CD132, CD86 or CD80 molecules on the surface of SACI-stimulated CD19(+) cells cul tured without or with AGC10. These results indicated that AGC10, derived fr om an organism that causes immunosuppression in infected hosts, down-regula tes B cell activities and suggested that the relevant mechanism could invol ve the molecular alterations described above. (C) 2001 Australian Society f or Parasitology Inc. Published by Elsevier Science Ltd. All rights reserved .