It is known that C3 is required for optimal expansion of T cells during acute viral infections. However, it is not yet determined whether T cell responses to intracellular bacterial infections require C3. Therefore, we have investigated the requirement for C3 to elicit potent T cell responses to Listeria monocytogenes (LM). We show that expansion of Ag-specific CD8 and CD4 T cells during a primary response to LM was markedly reduced in the absence of C3 activity. Further studies indicated that, unlike in an influenza virus infection, the regulation of LM-specific T cell responses by C3 might not involve the downstream effector C5a. Moreover, reduced T cell responses to LM was not linked to defective maturation of dendritic cells or developmental anomalies in the peripheral T cell compartment of C3-deficient mice. Experiments involving adoptive transfer of C3-deficient CD8 T cells into the C3-sufficient environment of wild-type mice showed that these T cells do not have intrinsic proliferative defects, and a paracrine source of C3 will suffice for clonal expansion of CD8 T cells in vivo. However, stimulation of purified C3-deficient CD8 T cells by plastic-immobilized anti-CD3 showed that C3 promotes T cell proliferation directly, independent of its effects on APC. On the basis of these findings, we propose that diminished T cell responses to LM in C3-deficient mice might be at least in part due to lack of direct effects of C3 on T cells. These studies have furthered our understanding of C3-mediated regulation of T cell immunity to intracellular pathogens.
%0 Journal Article
%1 Nakayama:2009jb
%A Nakayama, Yumi
%A Kim, Shin-Il
%A Kim, Eui Ho
%A Lambris, John D.
%A Sandor, Matyas
%A Suresh, M
%D 2009
%J Journal of Immunology
%K imported
%N 5
%P 2921--2931
%R 10.4049/jimmunol.0801191
%T C3 promotes expansion of CD8+ and CD4+ T cells in a Listeria monocytogenes infection.
%U http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19648268&retmode=ref&cmd=prlinks
%V 183
%X It is known that C3 is required for optimal expansion of T cells during acute viral infections. However, it is not yet determined whether T cell responses to intracellular bacterial infections require C3. Therefore, we have investigated the requirement for C3 to elicit potent T cell responses to Listeria monocytogenes (LM). We show that expansion of Ag-specific CD8 and CD4 T cells during a primary response to LM was markedly reduced in the absence of C3 activity. Further studies indicated that, unlike in an influenza virus infection, the regulation of LM-specific T cell responses by C3 might not involve the downstream effector C5a. Moreover, reduced T cell responses to LM was not linked to defective maturation of dendritic cells or developmental anomalies in the peripheral T cell compartment of C3-deficient mice. Experiments involving adoptive transfer of C3-deficient CD8 T cells into the C3-sufficient environment of wild-type mice showed that these T cells do not have intrinsic proliferative defects, and a paracrine source of C3 will suffice for clonal expansion of CD8 T cells in vivo. However, stimulation of purified C3-deficient CD8 T cells by plastic-immobilized anti-CD3 showed that C3 promotes T cell proliferation directly, independent of its effects on APC. On the basis of these findings, we propose that diminished T cell responses to LM in C3-deficient mice might be at least in part due to lack of direct effects of C3 on T cells. These studies have furthered our understanding of C3-mediated regulation of T cell immunity to intracellular pathogens.
@article{Nakayama:2009jb,
abstract = {It is known that C3 is required for optimal expansion of T cells during acute viral infections. However, it is not yet determined whether T cell responses to intracellular bacterial infections require C3. Therefore, we have investigated the requirement for C3 to elicit potent T cell responses to Listeria monocytogenes (LM). We show that expansion of Ag-specific CD8 and CD4 T cells during a primary response to LM was markedly reduced in the absence of C3 activity. Further studies indicated that, unlike in an influenza virus infection, the regulation of LM-specific T cell responses by C3 might not involve the downstream effector C5a. Moreover, reduced T cell responses to LM was not linked to defective maturation of dendritic cells or developmental anomalies in the peripheral T cell compartment of C3-deficient mice. Experiments involving adoptive transfer of C3-deficient CD8 T cells into the C3-sufficient environment of wild-type mice showed that these T cells do not have intrinsic proliferative defects, and a paracrine source of C3 will suffice for clonal expansion of CD8 T cells in vivo. However, stimulation of purified C3-deficient CD8 T cells by plastic-immobilized anti-CD3 showed that C3 promotes T cell proliferation directly, independent of its effects on APC. On the basis of these findings, we propose that diminished T cell responses to LM in C3-deficient mice might be at least in part due to lack of direct effects of C3 on T cells. These studies have furthered our understanding of C3-mediated regulation of T cell immunity to intracellular pathogens.},
added-at = {2017-12-08T05:18:19.000+0100},
affiliation = {Department of Pathobiological Sciences, University of Wisconsin, Madison, WI 53706, USA.},
author = {Nakayama, Yumi and Kim, Shin-Il and Kim, Eui Ho and Lambris, John D. and Sandor, Matyas and Suresh, M},
biburl = {https://www.bibsonomy.org/bibtex/21be3404a3aa5d63fda945c1cc5652eda/lambris},
date-added = {2012-03-27T20:48:59GMT},
date-modified = {2017-12-08T04:17:04GMT},
doi = {10.4049/jimmunol.0801191},
interhash = {a8fb290c4667abc23c9195e6a5dc0c8d},
intrahash = {1be3404a3aa5d63fda945c1cc5652eda},
journal = {Journal of Immunology},
keywords = {imported},
language = {English},
month = sep,
number = 5,
pages = {2921--2931},
pmcid = {PMC2753887},
pmid = {19648268},
rating = {0},
timestamp = {2017-12-08T05:18:19.000+0100},
title = {{C3 promotes expansion of CD8+ and CD4+ T cells in a Listeria monocytogenes infection.}},
uri = {\url{papers3://publication/doi/10.4049/jimmunol.0801191}},
url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19648268&retmode=ref&cmd=prlinks},
volume = 183,
year = 2009
}