Related Experiment Videos
Cell-mediated immunity in psoriatic arthritis
The Journal of Rheumatology
|March 1, 1980
Summary
Mitogen responses in psoriatic arthritis (PsA) patients were reduced, similar to active rheumatoid arthritis (RA). Lymphocyte responses improved as PsA disease activity decreased, indicating a link between immune function and disease severity.
Area of Science:
- Immunology
- Rheumatology
- Cellular Biology
Background:
- Psoriatic arthritis (PsA) is a chronic inflammatory disease.
- Immune system dysregulation is implicated in PsA pathogenesis.
- Mitogen-induced lymphocyte proliferation is a measure of immune cell function.
Purpose of the Study:
- To investigate the mitogen response of peripheral blood lymphocytes in patients with psoriatic arthritis (PsA).
- To compare lymphocyte responses in PsA patients with those in rheumatoid arthritis (RA) patients and healthy controls.
- To assess the relationship between mitogen response and disease activity in PsA.
Main Methods:
- Peripheral blood lymphocytes from 32 PsA patients, RA patients, and normal subjects were stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), and purified protein derivative (PPD).
- Lymphocyte proliferation was measured as an indicator of mitogen response.
- Sequential studies were conducted in a subset of PsA patients to correlate responses with disease activity.
Main Results:
- Mitogen responses (PHA, Con A, PWM) were significantly depressed in the PsA group compared to controls.
- The degree of mitogen response depression in PsA was comparable to that observed in active RA patients.
- In sequential studies, lymphocyte mitogen responses in PsA patients paralleled disease activity, increasing with disease improvement.
Conclusions:
- Lymphocyte mitogen responses are impaired in psoriatic arthritis, similar to active rheumatoid arthritis.
- The degree of immune cell dysfunction in PsA correlates with disease activity.
- These findings suggest a role for altered T-cell function in the immunopathogenesis of psoriatic arthritis.