| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Medicine, Division of Rheumatology, Mayo Clinic and Foundation, Rochester, MN 55905
T lymphocytes are a major component of the inflammatory infiltrate
in rheumatoid synovitis, but their exact role in the disease process is
not understood. Functional activities of synovial T cells were examined
by adoptive transfer experiments in human synovium-SCID mouse chimeras.
Adoptive transfer of tissue-derived autologous CD8+ T cells
induced a marked reduction in the activity of lesional T cells and
macrophages. Injection of CD8+, but not CD4+, T
cells decreased the production of tissue IFN-
, IL-1ß, and TNF-
by >90%. The down-regulatory effect of adoptively transferred
CD8+ T cells was not associated with depletion of synovial
CD3+ T cells or synovial CD68+ macrophages, and
it could be blocked by Abs against IL-16, a CD8+ T
cell-derived cytokine. In the synovial tissue, CD8+ T cells
were the major source of IL-16, a natural ligand of the CD4 molecule
that can anergize CD4-expressing cells. The anti-inflammatory
activity of IL-16 in rheumatoid synovitis was confirmed by treating
synovium-SCID mouse chimeras with IL-16. Therapy for 14 days with
recombinant human IL-16 significantly inhibited the production of
IFN-, IL-1ß, and TNF- in the synovium. We propose that
tissue-infiltrating CD8+ T cells in rheumatoid synovitis
have anti-inflammatory activity that is at least partially mediated
by the release of IL-16. Spontaneous production of IL-16 in synovial
lesions impairs the functional activity of CD4+ T cells but
is insufficient to completely abrogate their stimulation. Supplemental
therapy with IL-16 may be a novel and effective treatment for
rheumatoid arthritis.
This article has been cited by other articles:
|
|
 |
|
  M. D. Mannie and D. J. Abbott A Fusion Protein Consisting of IL-16 and the Encephalitogenic Peptide of Myelin Basic Protein Constitutes an Antigen-Specific Tolerogenic Vaccine That Inhibits Experimental Autoimmune Encephalomyelitis J. Immunol., August 1, 2007; 179(3): 1458 - 1465. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Davila, Y. M. Kang, Y. W. Park, H. Sawai, X. He, S. Pryshchep, J. J. Goronzy, and C. M. Weyand Cell-Based Immunotherapy with Suppressor CD8+ T Cells in Rheumatoid Arthritis J. Immunol., June 1, 2005; 174(11): 7292 - 7301. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X-J. Qin, H-Z. Shi, Z-X. Huang, L-F. Kang, W-N. Mo, and C. Wu Interleukin-16 in tuberculous and malignant pleural effusions Eur. Respir. J., April 1, 2005; 25(4): 605 - 611. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Pritchard, S. Tsui, N. Horst, W. W. Cruikshank, and T. J. Smith Synovial Fibroblasts from Patients with Rheumatoid Arthritis, Like Fibroblasts from Graves' Disease, Express High Levels of IL-16 When Treated with Igs against Insulin-Like Growth Factor-1 Receptor J. Immunol., September 1, 2004; 173(5): 3564 - 3569. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Elssner, A. I. Doseff, M. Duncan, M. Kotur, and M. D. Wewers IL-16 Is Constitutively Present in Peripheral Blood Monocytes and Spontaneously Released During Apoptosis J. Immunol., June 15, 2004; 172(12): 7721 - 7725. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. S. Prabhakar, R. S. Bahn, and T. J. Smith Current Perspective on the Pathogenesis of Graves' Disease and Ophthalmopathy Endocr. Rev., December 1, 2003; 24(6): 802 - 835. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Bannert, K. Vollhardt, B. Asomuddinov, M. Haag, H. Konig, S. Norley, and R. Kurth PDZ Domain-mediated Interaction of Interleukin-16 Precursor Proteins with Myosin Phosphatase Targeting Subunits J. Biol. Chem., October 24, 2003; 278(43): 42190 - 42199. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. M. Archin, L. van den Boom, L. Perelygina, J. M. Hilliard, and S. S. Atherton Delayed Spread and Reduction in Virus Titer after Anterior Chamber Inoculation of a Recombinant of HSV-1 Expressing IL-16 Invest. Ophthalmol. Vis. Sci., July 1, 2003; 44(7): 3066 - 3076. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Pritchard, R. Han, N. Horst, W. W. Cruikshank, and T. J. Smith Immunoglobulin Activation of T Cell Chemoattractant Expression in Fibroblasts from Patients with Graves' Disease Is Mediated Through the Insulin-Like Growth Factor I Receptor Pathway J. Immunol., June 15, 2003; 170(12): 6348 - 6354. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. P. Cope Exploring the reciprocal relationship between immunity and inflammation in chronic inflammatory arthritis Rheumatology, June 1, 2003; 42(6): 716 - 731. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M K Schuler, S Sell, and W K Aicher Protein kinase signals activate interleukin 16 encoding transcripts in rheumatoid arthritis versus osteoarthritis synovial fibroblasts Ann Rheum Dis, February 1, 2003; 62(2): 182 - 183. [Full Text] [PDF]
|
|
|
|
 |
|
 L R Lard, B O Roep, C A Verburgh, A H Zwinderman, and T W J Huizinga Elevated IL-16 levels in patients with systemic lupus erythematosus are associated with disease severity but not with genetic susceptibility to lupus Lupus, March 1, 2002; 11(3): 181 - 185. [Abstract] [PDF]
|
|
|
|
|
|
J. Pritchard, N. Horst, W. Cruikshank, and T. J. Smith Igs from Patients with Graves' Disease Induce the Expression of T Cell Chemoattractants in Their Fibroblasts J. Immunol., January 15, 2002; 168(2): 942 - 950. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Kaufmann, S. Franke, R. Kientsch-Engel, P. Oelzner, G. Hein, and G. Stein Correlation of circulating interleukin 16 with proinflammatory cytokines in patients with rheumatoid arthritis Rheumatology, April 1, 2001; 40(4): 474 - 475. [Full Text] [PDF]
|
|
|
|
|
|
E. Zanelli, F. C. Breedveld, and R. R. P. de Vries HLA association with autoimmune disease: a failure to protect? Rheumatology, October 1, 2000; 39(10): 1060 - 1066. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
