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*
Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and
Pulmonary Division, Johns Hopkins University School of Medicine, Baltimore, MD 21205
Ag presented by activated APCs promote immunogenic responses
whereas Ag presented by resting APCs leads to tolerance. In such a
model, the regulation of cytokine release by the presence or absence of
costimulation might potentially play a critical role in dictating the
ultimate outcome of Ag recognition. C-C chemokines are a structurally
defined family of chemoattractants that have diverse effects on
inflammation. We were interested in determining the activation
requirements for chemokine production by CD4+ T cells. Our
data demonstrate for T cell clones and previously activated T cells
from TCR-transgenic mice that stimulation with anti-TCR alone
results in the production of copious amounts of macrophage-inflammatory
protein-1
(MIP-1) and other C-C chemokines, and that addition of
anti-CD28 gives very little augmentation. Furthermore, MIP-1
production is nearly equivalent from both anergic and nonanergic cells.
For naive T cells, anti-CD3 stimulation alone led to as much
MIP-1 production as Ag + APC stimulation. The addition of
costimulation gave a 3–10-fold enhancement, but this was 70-fold less
than the effect of costimulation on IL-2 production. Thus, although C-C
chemokines play a broad role in influencing inflammation, their
production by signal 1 alone makes them unlikely to play a critical
role in the decision between a tolerogenic and an immunogenic response.
Furthermore, the production of MIP-1 by anergic T cells, as well as
following signal 1 alone, raises the possibility that in vivo this
chemokine serves to recruit activated T cells to become
tolerant.
This article has been cited by other articles:
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  T. Shin, G. Kennedy, K. Gorski, H. Tsuchiya, H. Koseki, M. Azuma, H. Yagita, L. Chen, J. Powell, D. Pardoll, et al. Cooperative B7-1/2 (CD80/CD86) and B7-DC Costimulation of CD4+ T Cells Independent of the PD-1 Receptor J. Exp. Med., July 7, 2003; 198(1): 31 - 38. [Abstract] [Full Text] [PDF]
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 R. O. Williams Cutting Edge: A-Kinase Anchor Proteins Are Involved in Maintaining Resting T Cells in an Inactive State J. Immunol., June 1, 2002; 168(11): 5392 - 5396. [Abstract] [Full Text] [PDF]
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