| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Department of Microbiology and
Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242
Inflammatory cytokines such as IFN-
and TNF produced by Ag-stimulated CD4+ and CD8+ T cells are important in defense against microbial infection. However, production of these cytokines must be tightly regulated to prevent immunopathology. Previous studies, conducted with BALB/c mice, have suggested that 1) CD8+ T cells maintain IFN- production but transiently produce TNF in the continued presence of Ag and 2) lymphocytic choriomeningitis virus-specific and in vitro-propagated effector CD8+ T cells could rapidly cycle IFN- production ON/OFF/ON in response to Ag exposure, removal, and re-exposure. In contrast with CD8+ T cells, our results show that Listeria monocytogenes-specific CD4+ T cells from C57BL/6 mice rapidly initiate (ON cycling) and maintain production of both IFN- and TNF in the continued presence of Ag. Upon Ag removal, production of both cytokines rapidly ceases (OFF cycling). However, if the initial stimulation was maximal, Ag-specific CD4+ T cells were unable to reinitiate cytokine production after a second Ag exposure. Furthermore, L. monocytogenes-specific CD8+ T cells in the same mice and lymphocytic choriomeningitis virus-specific CD8+ T cells in BALB/c mice also underwent ON/OFF cycling, but if the initial Ag stimulus was maximal, they could not produce IFN- after Ag re-exposure. As the initial Ag dose was reduced, the number of cells producing cytokine in response to the second Ag exposure exhibited a corresponding increase. However, T cells that were marked for IFN- secretion during the first stimulation did not contribute cytokine production during the second stimulation. Thus, T cells are not able to undergo rapid ON/OFF/ON cytokine cycling in vitro in response to Ag.
This article has been cited by other articles:
|
|
 |
|
  H. Maier, M. Isogawa, G. J. Freeman, and F. V. Chisari PD-1:PD-L1 Interactions Contribute to the Functional Suppression of Virus-Specific CD8+ T Lymphocytes in the Liver J. Immunol., March 1, 2007; 178(5): 2714 - 2720. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Virna, M. Deckert, S. Lutjen, S. Soltek, K. E. Foulds, H. Shen, H. Korner, J. D. Sedgwick, and D. Schluter TNF Is Important for Pathogen Control and Limits Brain Damage in Murine Cerebral Listeriosis J. Immunol., September 15, 2006; 177(6): 3972 - 3982. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Jabbari, K. L. Legge, and J. T. Harty T cell conditioning explains early disappearance of the memory CD8 T cell response to infection. J. Immunol., September 1, 2006; 177(5): 3012 - 3018. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Anghelina, L. Pewe, and S. Perlman Pathogenic Role for Virus-Specific CD4 T Cells in Mice with Coronavirus-Induced Acute Encephalitis Am. J. Pathol., July 1, 2006; 169(1): 209 - 222. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Storm, C. Bartholdy, M. R. Sorensen, J. P. Christensen, and A. R. Thomsen Perforin-Deficient CD8+ T Cells Mediate Fatal Lymphocytic Choriomeningitis despite Impaired Cytokine Production J. Virol., February 1, 2006; 80(3): 1222 - 1230. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Brehm, K. A. Daniels, and R. M. Welsh Rapid Production of TNF-{alpha} following TCR Engagement of Naive CD8 T Cells J. Immunol., October 15, 2005; 175(8): 5043 - 5049. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. D. Mayer, K. Mohrs, S. R. Crowe, L. L. Johnson, P. Rhyne, D. L. Woodland, and M. Mohrs The Functional Heterogeneity of Type 1 Effector T Cells in Response to Infection Is Related to the Potential for IFN-{gamma} Production J. Immunol., June 15, 2005; 174(12): 7732 - 7739. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
