Loading…

Mouse splenic CD4 super(+) and CD8 super(+) T cells undergo extensive apoptosis during a Plasmodium chabaudi chabaudi AS infection

The presence and phenotype of apoptotic lymphocytes was studied in spleen cell suspensions taken from CB6F1 mice infected with Plasmodium chabaudi chabaudi AS. High levels of apoptotic cells were found, associated with high parasitaemias and splenomegaly. This was also accompanied by expansion and d...

Full description

Saved in:
Bibliographic Details
Published in:Parasite immunology 2001-12, Vol.23 (12), p.617-626
Main Authors: Sanchez-Torres, L, Rodriguez-Ropon, A, Aguilar-Medina, M, Favila-Castillo, L
Format: Article
Language:English
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The presence and phenotype of apoptotic lymphocytes was studied in spleen cell suspensions taken from CB6F1 mice infected with Plasmodium chabaudi chabaudi AS. High levels of apoptotic cells were found, associated with high parasitaemias and splenomegaly. This was also accompanied by expansion and disarray of spleen white pulp. Apoptosis levels lowered when parasitaemia was cleared, but were still higher than in normal mice. At this time, the spleen was diminishing in size and the white pulp was contracting and rearranging. When parasitaemia was patent, the cells most affected by apoptosis were CD4 super(+) T cells followed by CD8 super(+) T cells, and to a lesser extent B220 super(+) B cells. When parasitaemia was cleared, CD8 super(+) T cells and B220 super(+) B cells returned to basal levels of apoptosis, while CD4 super(+) T cells still had higher apoptosis levels than normal mice. A similar pattern of lymphocyte subpopulation apoptosis was found in infected BALB/c mice, despite the fact that, for this mouse model, it has been reported that B cells are the cells that are most affected by apoptosis. We consider that the high levels of apoptosis in CD4 super(+) T cells when parasitaemias are still high are not easily explained by a normal mechanism of down regulation of the immune response.
ISSN:0141-9838
DOI:10.1046/j.1365-3024.2001.00422.x