Altered T cell subpopulations and lymphocytes expressing natural killer cell phenotypes in patients with progressive systemic sclerosis. 1991

M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
Department of Pathology, Nassau County Medical Center, State University of New York at Stony Brook, East Meadow.

Scleroderma (progressive systemic sclerosis [PSS]) is known to be associated with abnormal T cell immunoregulation. In the present study, we evaluated lymphocyte phenotypes in patients with PSS and normal control subjects by flow cytometry and monoclonal antibodies for total T (CD3), T suppressor (CD8), T helper (CD4), T helper-inducer (CDw29), T suppressor-inducer (CD45R), human leukocyte antigen, DR+B (CD19), DR+T, and natural killer subsets, HNK-1 (CD57) and NKH-1 (CD56) cells. Patients with PSS compared to normal subjects had significantly lower percentages of CD3+ (p less than 0.005) and CD8+ (p less than 0.05) (similar to several patients with rheumatoid arthritis also evaluated), as well as CD45R (p less than 0.05), T+DR+ (p less than 0.05), and NKH-1 (CD56) (p less than 0.0005) cells. Patients with PSS with late-limited or generalized disease had lower percentages of CD8+, CD19, NKH-1+, and CDw29, but higher percentages of CD4+, HNK-1, and CD45R cells compared to patients with early stage disease, but these results were not statistically significant. These unique alterations in patients with PSS may prove to be useful in monitoring the stage of disease activity for therapy and further define immunologic defects.

UI MeSH Term Description Entries
D007694 Killer Cells, Natural Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type. NK Cells,Natural Killer Cells,Cell, NK,Cell, Natural Killer,Cells, NK,Cells, Natural Killer,Killer Cell, Natural,NK Cell,Natural Killer Cell
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D010641 Phenotype The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment. Phenotypes
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults
D000368 Aged A person 65 years of age or older. For a person older than 79 years, AGED, 80 AND OVER is available. Elderly
D001172 Arthritis, Rheumatoid A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated. Rheumatoid Arthritis
D012595 Scleroderma, Systemic A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA. Sclerosis, Systemic,Systemic Scleroderma,Systemic Sclerosis

Related Publications

M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
November 1979, Clinical and experimental immunology,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
July 1983, Arthritis and rheumatism,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
June 1992, Arthritis and rheumatism,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
September 1975, The Journal of rheumatology,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
January 1994, Virchows Archiv : an international journal of pathology,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
October 2019, Arthritis research & therapy,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
February 2005, The Journal of rheumatology,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
January 2012, PloS one,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
January 1984, Acta haematologica,
M Frieri, and C Angadi, and A Paolano, and N Oster, and S P Blau, and S Yang, and C Mele, and E Hawrylko
January 1985, Acta medica Hungarica,
Copied contents to your clipboard!