Decreased expression of CD7 occurs in rheumatoid arthritis

To evaluate the possibility of antigenic modulation in vivo, we studied the expression of the CD7 antigen on the surface of peripheral blood and intrasynovial lymphocytes from patients with rheumatoid arthritis (RA). This disease is noted for features predicting changes in CD7: (1) increased express...

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Bibliographic Details
Published in:Clinical and experimental immunology 1988-06, Vol.72 (3), p.470-475
Main Authors: LAZAROVITS, A. I, KARSH, J
Format: Article
Language:English
Subjects:
Adult
Antigens, Surface - analysis
Arthritis, Rheumatoid - immunology
Biological and medical sciences
Diseases of the osteoarticular system
Female
Flow Cytometry
Humans
Immunoenzyme Techniques
Inflammatory joint diseases
Lymphocyte Activation
Male
Medical sciences
Middle Aged
Synovial Membrane - immunology
T-Lymphocytes - immunology
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Summary:To evaluate the possibility of antigenic modulation in vivo, we studied the expression of the CD7 antigen on the surface of peripheral blood and intrasynovial lymphocytes from patients with rheumatoid arthritis (RA). This disease is noted for features predicting changes in CD7: (1) increased expression related to activation during an immune response through possible contact with 'disease associated antigens' and (2) decreased expression associated with lymphocytes moving through tissue. We found a highly significant decrease of CD7 on RA T cells in vivo (P less than 10(-4] that was not related to disease activity, drug ingestion, or abnormalities in the ability of RA T cells to express or modulate the antigen in vitro. Similar decreased expression was observed on many intrasynovial T cells that were nevertheless activated as measured by expression of activation markers such as Act I (a late lymphocyte activation antigen) and Act II (the transferrin receptor). Decreased expression of CD7 occurs naturally in vivo in RA; this observation may have future significance in better understanding the immunopathogenesis of this disease.
ISSN:0009-9104
1365-2249