Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Chemokines CCL19 and CCL21 promote activation-induced cell death of antigen-responding T cells

Item Type:Article
Title:Chemokines CCL19 and CCL21 promote activation-induced cell death of antigen-responding T cells
Creators Name:Yasuda, T., Kuwabara, T., Nakano, H., Aritomi, K., Onodera, T., Lipp, M., Takahama, Y. and Kakiuchi, T.
Abstract:Secondary lymphoid organs (SLOs) provide a niche for the initiation and regulation of T cell responses, but the mechanisms have been poorly understood. We investigated the influence of chemokines CCL19 and CCL21 constitutively expressed in SLOs on activation-induced cell death (AICD) of CD4(+) T cells. When paucity of lymph node T cells (plt) mutant mice lacking expression of CCL19/CCL21 were primed with OVA/CFA, both expansion of OVA-responding CD4(+) T cells in the draining lymph nodes and an in vitro recall-response were prolonged as compared with responses in wild type (WT) mice. The apoptotic cell frequency among OVA-responding CD4(+) T cells was similarly low in plt/plt and WT mice during clonal expansion phase. However, during the clonal contraction phase, the frequency never increased in plt/plt mice, whereas in WT mice it continuously increased to a peak 18 days after immunization. The presence of CCL19/CCL21 during the in vitro stimulation of CD4(+) T cells with anti-CD3+anti-CD28 significantly enhanced in vitro AICD induction of the restimulated T cells, partially through enhancing Fas-ligand expression. Our results suggest that CCL19/CCL21 produced by stromal cells and antigen-presenting cells regulate CD4(+) T cell immune responses in SLOs by promoting AICD.
Keywords:Chemokine, CCL19, CCL21, T cell, Apoptosis, plt mouse, Activation-induced cell death, Animals, Mice
Source:Blood
ISSN:0006-4971
Publisher:American Society of Hematology
Volume:109
Number:2
Page Range:449-456
Date:15 January 2007
Official Publication:https://doi.org/10.1182/blood-2006-04-018101
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library