Giuseppe
Emeritus
Recruited inflammatory monocytes stimulate antiviral Th1 immunity in infected tissue (PNAS, abstract, edited)
[Source: Proc Natl Acad Sci USA, full text: <cite cite="http://www.pnas.org/content/108/1/284.short?rss=1">Recruited inflammatory monocytes stimulate antiviral Th1 immunity in infected tissue ? PNAS</cite>. Abstract, edited.]
Recruited inflammatory monocytes stimulate antiviral Th1 immunity in infected tissue
1. Norifumi Iijima, 2. Lisa M. Mattei, and 3. Akiko Iwasaki 1
Author Affiliations
1. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520
1. Edited by Laurie H. Glimcher, Harvard School of Public Health, Boston, MA, and approved December 1, 2010 (received for review April 16, 2010)
Abstract
Monocytes patrol various tissues for signs of infection and inflammation. Inflammatory monocytes enter peripheral tissues at sites of microbial infection and differentiate into dendritic cells and macrophages. Here, we examined the importance of monocytes in primary mucosal infection with herpes simplex virus 2 (HSV-2), and demonstrate that monocyte-derived APCs are required to elicit IFN-γ secretion from effector Th1 cells to mediate antiviral protection. However, monocyte-derived APCs were dispensable for the generation of Th1 immunity and for the restimulation of memory Th1 cells during secondary viral challenge. These results demonstrate that distinct APC subsets are dedicated for CD4 T cell priming, elicitation, and memory recall responses to a given viral pathogen within the same mucosal tissue and reveal a specialized role for monocyte-derived APCs in the emergency response to infection.
* migration
* sexually transmitted infection
* antigen presentation
Footnotes
* 1 To whom correspondence should be addressed. E-mail: akiko.iwasaki@yale.edu.
* Author contributions: N.I. and A.I. designed research; N.I. and L.M.M. performed research; N.I. and A.I. analyzed data; and N.I. and A.I. wrote the paper.
* The authors declare no conflict of interest.
* This article is a PNAS Direct Submission.
* This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1005201108/-/DCSupplemental.
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[Source: Proc Natl Acad Sci USA, full text: <cite cite="http://www.pnas.org/content/108/1/284.short?rss=1">Recruited inflammatory monocytes stimulate antiviral Th1 immunity in infected tissue ? PNAS</cite>. Abstract, edited.]
Recruited inflammatory monocytes stimulate antiviral Th1 immunity in infected tissue
1. Norifumi Iijima, 2. Lisa M. Mattei, and 3. Akiko Iwasaki 1
Author Affiliations
1. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520
1. Edited by Laurie H. Glimcher, Harvard School of Public Health, Boston, MA, and approved December 1, 2010 (received for review April 16, 2010)
Abstract
Monocytes patrol various tissues for signs of infection and inflammation. Inflammatory monocytes enter peripheral tissues at sites of microbial infection and differentiate into dendritic cells and macrophages. Here, we examined the importance of monocytes in primary mucosal infection with herpes simplex virus 2 (HSV-2), and demonstrate that monocyte-derived APCs are required to elicit IFN-γ secretion from effector Th1 cells to mediate antiviral protection. However, monocyte-derived APCs were dispensable for the generation of Th1 immunity and for the restimulation of memory Th1 cells during secondary viral challenge. These results demonstrate that distinct APC subsets are dedicated for CD4 T cell priming, elicitation, and memory recall responses to a given viral pathogen within the same mucosal tissue and reveal a specialized role for monocyte-derived APCs in the emergency response to infection.
* migration
* sexually transmitted infection
* antigen presentation
Footnotes
* 1 To whom correspondence should be addressed. E-mail: akiko.iwasaki@yale.edu.
* Author contributions: N.I. and A.I. designed research; N.I. and L.M.M. performed research; N.I. and A.I. analyzed data; and N.I. and A.I. wrote the paper.
* The authors declare no conflict of interest.
* This article is a PNAS Direct Submission.
* This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1005201108/-/DCSupplemental.
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