Premium
Impaired Mitogen‐Induced Interferon‐γ Production in Rheumatoid Arthritis and Related Diseases
Author(s) -
STOLZENBURG T.,
BINZ H.,
FONTANA A.,
FELDER M.,
WAGENHAEUSER F.J.
Publication year - 1988
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1988.tb02324.x
Subject(s) - phytohaemagglutinin , rheumatoid arthritis , pokeweed mitogen , medicine , concanavalin a , immunology , stimulation , interleukin 2 , endocrinology , interferon gamma , interferon , arthritis , cytokine , biology , in vitro , biochemistry
Peripheral blood lymphocytes from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), progressive systemic sclerosis (PSS). Reiter's disease, osteoarthritis, and from healthy volunteers were investigated for interferon‐γ (IFN‐γ) production after mitogen activation. Phytohaemagglutinin stimulation revealed an impaired IFN‐γ production in RA, SLE, and PSS but normal levels to Reiter's disease and osteoarthritis. In RA this deficiency was also seen after pokeweed mitogen. OKT3, and concanavalin A activation. No major differences were found in interleukin 2 (IL‐2) production and cell proliferation. The IL‐2 receptor expression was reduced on stimulated RA lymphocytes. The deficient IFN‐γ production was compensated in RA by co stimulation of PHA or OKT3 with phorbol myristic acetate (PMA). In addition, the combination of the calcium ionophore A 23187 and PMA induced a strong IFN‐γ secretion in all patient groups and in the controls.