IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cardona, A. E.
Right arrow Articles by Teale, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cardona, A. E.
Right arrow Articles by Teale, J. M.

 Previous Article  |  Next Article 

Infection and Immunity, May 2003, p. 2634-2642, Vol. 71, No. 5
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.5.2634-2642.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

CC Chemokines Mediate Leukocyte Trafficking into the Central Nervous System during Murine Neurocysticercosis: Role of {gamma}{delta} T Cells in Amplification of the Host Immune Response

Astrid E. Cardona, Paula A. Gonzalez, and Judy M. Teale*

Department of Microbiology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229

Received 22 May 2002/ Returned for modification 18 July 2002/ Accepted 14 February 2003

According to a previous report, the degree of the host immune response highly correlates with severity of the disease in the murine model for neurocysticercosis. In wild-type mice, Mesocestoides corti infection induced a rapid and extensive accumulation of {gamma}{delta} T cells and macrophages in the brain. NK cells, dendritic cells, {alpha}ß T cells, and B cells were also recruited to the brain but at lower levels. In contrast, {gamma}{delta} T-cell-deficient mice exhibited decreased cellular infiltration and reduced central nervous system (CNS) pathology. To understand the mechanisms of leukocyte recruitment into the CNS, chemokine expression was analyzed in infected brains in the present study. MCP-1 (CCL2), MIP-1{alpha} (CCL3), and MIP-1ß (CCL4) were up-regulated within 2 days after M. corti infection. Protein expression of RANTES (CCL5), eotaxin (CCL11), and MIP-2 was detected later, at 1 week postinfection. Correlating with the decreased cellular infiltration, delta chain T-cell receptor-deficient (TCR{delta}-/-) mice exhibited substantially reduced levels of most of the chemokines analyzed (with the exception of eotaxin). The results suggest that {gamma}{delta} T cells play an important role in the CNS immune response by producing chemokines such as MCP-1 and MIP-1{alpha}, enhancing leukocyte trafficking into the brain during murine neurocysticercosis.

* Corresponding author. Mailing address: Department of Microbiology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229. Phone: (210) 657-3959. Fax: (210) 567-6612. E-mail: teale{at}uthscsa.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, May 2003, p. 2634-2642, Vol. 71, No. 5
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.5.2634-2642.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2003 by the American Society for Microbiology. All rights reserved.