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Differential effects of Trypanosoma cruzi on the transcription of the p55IL‐2R, c‐fos, c‐myc and CD69 genes in activated human lymphocytes
Author(s) -
KIERSZENBAUM F.,
MAJUMDER S.,
LOPEZ H. MEJIA,
SZTEIN M. B.
Publication year - 1995
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1995.tb00889.x
Subject(s) - phytohaemagglutinin , biology , trypanosoma cruzi , transcription (linguistics) , microbiology and biotechnology , peripheral blood mononuclear cell , messenger rna , gene expression , gene , immune system , immunology , parasite hosting , biochemistry , in vitro , linguistics , philosophy , world wide web , computer science
Summary Mitogen‐activated lymphocytes co‐cultured with either purified Trypanosoma cruzi trypomastigotes or the filtrate of trypomastigote suspensions in culture medium manifest a significant decrease in their capacities to express p55 interleukin‐2 receptor molecules (p55IL‐2R) on their membrane and proliferate. In this study we found that the cytoplasmic levels of p55IL‐2R are also markedly reduced under these conditions. This inhibition appeared to result from altered gene transcription since the levels of p55IL‐2R mRNA in phytohaemagglutinin (PHA)‐stimulated human peripheral blood mononuclear cells (PBMC) dropped substantially in the presence of parasite suspension filtrate. The rates of decay for p55IL‐2R mRNA determined in cultures lacking and containing the parasite filtrate after addition of actinomycin D to inhibit further RNA synthesis were comparable. These results indicated that decreased p55IL‐2R mRNA was not due to decreased stability of this mRNA under our conditions and pointed to a transcriptional or pre‐transcriptional modification as the likely mechanism by which T. cruzi affects activated lymphocytes. The parasite filtrate did not appear to affect transcription of c‐fos or c‐myc (known to occur in the very early stages of lymphocyte activation) or that of CD69 (which is concomitant with p55IL‐2R transcription). Thus, decreased p55IL‐2R gene transcription appears to be a somewhat selective effect of a T. cruzi‐derived molecule(s) rather than the consequence of an overall shutdown of gene transcription.