Related Experiment Video
Updated: Jan 30, 2026

Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice
Published on: October 27, 2023
Lymphocyte aberrations in ankylosing spondylitis
Abstract:
Because the etiology of IgA and IgG hyperimmunoglobulinemia in ankylosing spondylitis (AS) remains unknown, the cellular immune system has been further studied by measuring the lymphocyte and its subpopulations in peripheral bloods of 50 definite AS patients and 40 normal controls. The system's functions have also been assessed in terms of proliferative responses to phytomitogens (Con A, PHA and PWM) and autologous mixed lymphocyte reaction (AMLR). The following results were obtained: The number of lymphocytes, total T, active T, OKIa1, OKT3, OKT4 and OKT8 cells in peripheral bloods of AS patients decreased more significantly when compared to the normal controls. The ratio of OKT4/OKT8 also decreased. However, the number of OKT8 cells was normal in inactive stage. While the lymphocytes of AS responded hyperreactively to PWM (B-cell mitogen), the response to Con A (T-cell mitogen) was depressed significantly. AMLR was impaired in AS patients no matter whether monocytes or B cells were used as stimulators. The aforementioned changes were especially evident in the active stage and most of them returned to normal after the disease became quiescent. It is therefore concluded that the etiology of hyperreactivity of B-cells in AS may be caused by T-cell immune aberration as evidenced by depressed lymphoproliferative response to T-cell mitogen (Con A) and impaired AMLR and/or the hyperfunction of B-cells themselves.
Related Concept Videos
Nucleotide Excision Repair
DNA-only Transposons
The donor site from where the transposon is excised is either degraded or...
Amyloid Fibrils
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
What is the Immune System?
Vaccinations
Inflammation

