Clonal dominance among T-lymphocyte infiltrates in arthritis

Journal Article · Mon Feb 01 04:00:00 EST 1988 · Proc. Natl. Acad. Sci. U.S.A.; (United States)

DOI:https://doi.org/10.1073/pnas.85.4.1179· OSTI ID:6652115

Stamenkovic, I; Stegagno, M; Wright, K A; Krane, S M; Amento, E P; Colvin, R B; Duquesnoy, R J; Kurnick, J T

Synovial membranes in patients with rheumatoid arthritis as well as other types of chronic destructive inflammatory arthritis contain infiltrates of activated T lymphocytes that probably contribute to the pathogenesis of the disease. In an effort to elucidate the nature of these infiltrates, interleukin 2 (IL-2)-responsive T lymphocytes were grown out of synovial fragments from 14 patients undergoing surgery for advanced destructive inflammatory joint disease. Eleven of the samples examined were from patients with classical rheumatoid arthritis, while three others were obtained from individuals with clinical osteoarthritis. Southern blot analysis of T-cell receptor (TCR) ..beta..-chain genes in 13 of 14 cultures showed distinct rearrangements, indicating that each culture was characterized by the predominance of a limited number of clones. T-cell populations from peripheral blood stimulated with a variety of activators and expanded with IL-2 did not demonstrate evidence of similar clonality in long-term culture. These results suggest that a limited number of activated T-cell clones predominate at the site of tissue injury in rheumatoid synovial membranes as well as in other types of destructive inflammatory joint disease. Further characterization of these T-cell clones may aid our understanding of the pathogenesis of these rheumatic disorders.

• Research Organization: Harvard Medical School, Boston, MA (USA)
• OSTI ID: 6652115
• Journal Information: Proc. Natl. Acad. Sci. U.S.A.; (United States), Journal Name: Proc. Natl. Acad. Sci. U.S.A.; (United States) Vol. 85:4; ISSN PNASA
• Country of Publication: United States
• Language: English

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59 BASIC BIOLOGICAL SCIENCES
ANIMAL CELLS
ANTIBODIES
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BIOLOGICAL MATERIALS
BLOOD
BLOOD CELLS
BODY FLUIDS
CELL PROLIFERATION
CONNECTIVE TISSUE CELLS
DAYS LIVING RADIOISOTOPES
DISEASES
GROWTH FACTORS
INFLAMMATION
ISOTOPES
LEUKOCYTES
LIGHT NUCLEI
LYMPHOCYTES
LYMPHOKINES
MATERIALS
MEMBRANE PROTEINS
MITOGENS
MOLECULAR STRUCTURE
MONOCLONAL ANTIBODIES
NUCLEI
ODD-ODD NUCLEI
ORGANIC COMPOUNDS
PATHOGENESIS
PATHOLOGICAL CHANGES
PATIENTS
PHOSPHORUS 32
PHOSPHORUS ISOTOPES
PROTEINS
RADIOISOTOPES
RECEPTORS
RHEUMATIC DISEASES
SKELETAL DISEASES
SOMATIC CELLS
SYMPTOMS