Abstract
PKC-θ is central to T-helper (Th) 2 cell differentiation and effector function; however, its importance for antiviral effector, and in particular memory CD8+ T cell responses, remains unclear. We have investigated the role of PKC-θ during in vivo and in vitro responses against influenza virus, lymphocytic choriomeningitis virus, vaccinia virus, and replication-deficient virus-like particles. In the absence of PKC-θ, antiviral CD8+ T cells presented an unresponsive phenotype in vitro, which could be restored with exogenous IL-2 or by Toll-like receptor ligand-activated dendritic cells. In striking contrast, PKC-θ appeared to be superfluous for in vivo antiviral responses irrespective of whether the virus infected systemically, was localized to the lung, or did not replicate. In addition, CD8+ CCR7-effector memory responses were normal in PKC-θ-deficient mice, both in lymphoid and peripheral tissues. Our data show that increased activation signals delivered in vivo by highly activated dendritic cells, as present during viral infections, overcome the requirement for PKC-θ during CD8+ T cell antiviral responses.
| Original language | English |
|---|---|
| Pages (from-to) | 14374-14379 |
| Number of pages | 6 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 102 |
| Issue number | 40 |
| DOIs | |
| Publication status | Published - 4 Oct 2005 |
| Externally published | Yes |
Keywords
- Protein kinase C
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Innate signals compensate for the absence of PKC-θ during in vivo CD8+ T cell effector and memory responses. / Marsland, Benjamin J.; Nembrini, Chiara; Schmitz, Nicole; Abel, Brian; Krautwald, Stefan; Bachmann, Martin F.; Kopf, Manfred.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 102, No. 40, 04.10.2005, p. 14374-14379.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Innate signals compensate for the absence of PKC-θ during in vivo CD8+ T cell effector and memory responses
AU - Marsland, Benjamin J.
AU - Nembrini, Chiara
AU - Schmitz, Nicole
AU - Abel, Brian
AU - Krautwald, Stefan
AU - Bachmann, Martin F.
AU - Kopf, Manfred
PY - 2005/10/4
Y1 - 2005/10/4
N2 - PKC-θ is central to T-helper (Th) 2 cell differentiation and effector function; however, its importance for antiviral effector, and in particular memory CD8+ T cell responses, remains unclear. We have investigated the role of PKC-θ during in vivo and in vitro responses against influenza virus, lymphocytic choriomeningitis virus, vaccinia virus, and replication-deficient virus-like particles. In the absence of PKC-θ, antiviral CD8+ T cells presented an unresponsive phenotype in vitro, which could be restored with exogenous IL-2 or by Toll-like receptor ligand-activated dendritic cells. In striking contrast, PKC-θ appeared to be superfluous for in vivo antiviral responses irrespective of whether the virus infected systemically, was localized to the lung, or did not replicate. In addition, CD8+ CCR7-effector memory responses were normal in PKC-θ-deficient mice, both in lymphoid and peripheral tissues. Our data show that increased activation signals delivered in vivo by highly activated dendritic cells, as present during viral infections, overcome the requirement for PKC-θ during CD8+ T cell antiviral responses.
AB - PKC-θ is central to T-helper (Th) 2 cell differentiation and effector function; however, its importance for antiviral effector, and in particular memory CD8+ T cell responses, remains unclear. We have investigated the role of PKC-θ during in vivo and in vitro responses against influenza virus, lymphocytic choriomeningitis virus, vaccinia virus, and replication-deficient virus-like particles. In the absence of PKC-θ, antiviral CD8+ T cells presented an unresponsive phenotype in vitro, which could be restored with exogenous IL-2 or by Toll-like receptor ligand-activated dendritic cells. In striking contrast, PKC-θ appeared to be superfluous for in vivo antiviral responses irrespective of whether the virus infected systemically, was localized to the lung, or did not replicate. In addition, CD8+ CCR7-effector memory responses were normal in PKC-θ-deficient mice, both in lymphoid and peripheral tissues. Our data show that increased activation signals delivered in vivo by highly activated dendritic cells, as present during viral infections, overcome the requirement for PKC-θ during CD8+ T cell antiviral responses.
KW - Protein kinase C
UR - http://www.scopus.com/inward/record.url?scp=26444476013&partnerID=8YFLogxK
U2 - 10.1073/pnas.0506250102
DO - 10.1073/pnas.0506250102
M3 - Article
VL - 102
SP - 14374
EP - 14379
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 40
ER -