| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Department of Genetics,
Department of Microbiology, and
Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294
Mac-1 (CD18/CD11b) is a member of the 
2-integrin family of adhesion molecules and is implicated in the development of many inflammatory diseases. The role of Mac-1 in the development of CNS demyelinating diseases, including multiple sclerosis, is not understood, and Ab inhibition studies in experimental allergic encephalomyelitis (EAE), the animal model for multiple sclerosis, have produced conflicting findings. To clarify these results and to determine Mac-1-mediated mechanisms in EAE, we performed EAE using Mac-1-deficient mice. Mac-1 homozygous-deficient, but not Mac-1 heterozygous-deficient mice, had significantly delayed onset and attenuated EAE. Leukocyte infiltration was similar in both groups of mice in early disease but significantly reduced in spinal cords of receptor-deficient mice in late disease. Adoptive transfer of Ag-restimulated T cells from wild-type to Mac-1-deficient mice produced significantly attenuated EAE, whereas transfer of Mac-1-deficient Ag-restimulated T cells to control mice failed to induce EAE. T cells from myelin oligodendrocyte glycoprotein (MOG)35–55 peptide-primed Mac-1-deficient mice displayed an altered cytokine phenotype with elevated levels of TGF- and IL-10, but reduced levels of IL-2, IFN-
, TNF-
, IL-12, and IL-4 compared with control mice. Mac-1-deficient T cells from primed mice proliferated comparably to that of control T cells on MOG35–55 restimulation in vitro. However, the draining lymph nodes of MAC-1-deficient mice on day 10 after MOG35–55 immunization contained lower frequency of blast T cells than in control mice, suggesting poor priming. Our results indicate that Mac-1 expression is critical on both phagocytic cells and T cells for the development of demyelinating disease.
This article has been cited by other articles:
|
|
 |
|
  A. Goncalves DaSilva and V. W. Yong Matrix Metalloproteinase-12 Deficiency Worsens Relapsing-Remitting Experimental Autoimmune Encephalomyelitis in Association with Cytokine and Chemokine Dysregulation Am. J. Pathol., March 1, 2009; 174(3): 898 - 909. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R.-N. E. Dogan, A. Elhofy, and W. J. Karpus Production of CCL2 by Central Nervous System Cells Regulates Development of Murine Experimental Autoimmune Encephalomyelitis through the Recruitment of TNF- and iNOS-Expressing Macrophages and Myeloid Dendritic Cells J. Immunol., June 1, 2008; 180(11): 7376 - 7384. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Stapulionis, C. L. Pinto Oliveira, M. C. Gjelstrup, J. S. Pedersen, M. E. Hokland, S. V. Hoffmann, K. Poulsen, C. Jacobsen, and T. Vorup-Jensen Structural Insight into the Function of Myelin Basic Protein as a Ligand for Integrin {alpha}M{beta}2 J. Immunol., March 15, 2008; 180(6): 3946 - 3956. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. S. Smith and S. R. Barnum Differential expression of {beta}2-integrins and cytokine production between {gamma}{delta} and {alpha}{beta} T cells in experimental autoimmune encephalomyelitis J. Leukoc. Biol., January 1, 2008; 83(1): 71 - 79. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. V. Ostanin, K. L. Furr, K. P. Pavlick, L. Gray, C. G. Kevil, D. Shukla, D. D'Souza, J. M. Hoffman, and M. B. Grisham T cell-associated CD18 but not CD62L, ICAM-1, or PSGL-1 is required for the induction of chronic colitis Am J Physiol Gastrointest Liver Physiol, June 1, 2007; 292(6): G1706 - G1714. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Bullard, X. Hu, J. E. Adams, T. R. Schoeb, and S. R. Barnum p150/95 (CD11c/CD18) Expression Is Required for the Development of Experimental Autoimmune Encephalomyelitis Am. J. Pathol., June 1, 2007; 170(6): 2001 - 2008. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
