Abstract |
The present study describes a novel experimental immunotherapeutic methodology for the reduction of inflammatory synovitis that is noted in an animal model of rheumatoid arthritis. The reduction in inflammation is noted in the animals administered a contra-interleukin-2 (IL-2) cytokine secreted by a cloned T-cell line. The mechanism of reduction of inflammation by this cytokine is through the inhibition of activation and differentiation of T lymphocytes. The cytokine inhibits the in vitro mitogen activation of T-cell lymphocytes as well as antigen-specific activation of a collagen type II specific T-cell line. In addition, decreased levels of messenger RNA coding for interleukin-2 are noted in T lymphocytes and IL-2 activation of the collagen type II specific cell line is inhibited by the contra-IL-2 cytokine. This initial description of a reduction in inflammation by a contra-IL-2 lymphokine suggests that immunoregulatory biologic molecules that are antagonists to IL-2 may be useful for the experimental immunotherapy of cartilage connective tissue pathology.
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Authors | D J Spannaus-Martin, R Holmdahl, T F Kresina |
Journal | The American journal of pathology
(Am J Pathol)
Vol. 137
Issue 2
Pg. 331-9
(Aug 1990)
ISSN: 0002-9440 [Print] United States |
PMID | 2201199
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Biological Factors
- Cytokines
- Interleukin-2
- RNA, Messenger
- Collagen
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Topics |
- Animals
- Arthritis
(drug therapy)
- Arthritis, Experimental
(chemically induced, drug therapy, metabolism)
- Biological Factors
(pharmacology, therapeutic use)
- Blast Crisis
(pathology)
- Cell Differentiation
(drug effects)
- Cell Line
- Collagen
- Cytokines
- Hybridomas
(metabolism, pathology)
- Interleukin-2
(antagonists & inhibitors, genetics, metabolism)
- Lymphocyte Activation
(drug effects)
- Male
- Mice
- RNA, Messenger
(drug effects, genetics, metabolism)
- T-Lymphocytes
(cytology, metabolism)
- Thymoma
(metabolism, pathology)
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