M. Kodera et al., Involvement of apoptosis in activation-induced cell death of bacteria-reactive human CD45RO+T cells, RES COM M P, 104(2), 1999, pp. 205-218
Citations number
31
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
RESEARCH COMMUNICATIONS IN MOLECULAR PATHOLOGY AND PHARMACOLOGY
Although the identity of the T cells that protect against bacteria in human
s remains unknown, it is clear that patients with bacterial infection have
reduced numbers of T cells in their blood. Here we have determined whether
this T cell loss is a consequence of bacterial antigen-mediated activation-
induced cell death (AICD). By flowcytometric analysis, less than 0.3% of fr
eshly isolated T cells from healthy volunteers and patients with severe pne
umonia were identified as apoptotic. However, during culture the rate of ap
optosis in peripheral blood T cells from patients was 3.0 +/- 0.9%; and inc
reased further in the presence of anti-CD3 (7.4 +/- 2.1%) and decreased whe
n IL-2 was added (4.4 +/- 1.3%). In contrast, no changes were observed in h
ealthy volunteers on addition of anti-CD3. Further, anti-CD3 significantly
increased the susceptibility to apoptosis of CD45RO+ T cells, but not CD45R
A+ T cells from patients, and the percentage of CD45RO+ T cells in patients
was significantly higher than that in healthy volunteers. Flowcytometric a
nalysis revealed the expression level of Fas to be higher in the patients t
han healthy volunteers. Collectively, these findings demonstrated that bact
eria-reactive T cells were more susceptible to AICD and that Fas-FasL pathw
ays of apoptosis were involved. AICD of CD45RO+ T cells, therefore, provide
s an explanation for the loss of bacteria-reactive T cells during bacterial
infection.