T lymphocytes in ankylosing spondylitis and the influence of sulphasalazine treatment

Abstract

Twenty-nine patients with ankylosing spondylitis (AS) were studied in an attempt to evaluate the role of T lymphocytes in this disease and a possible influence of treatment. The proportions of various T cell subpopulations in blood were assessed with monoclonal antibodies. Before treatment the proportions of Leu-4+ cells and Leu 3a+ cells were decreased while Leu-2a+ lymphocytes appeared in normal proportions. Leu-7+ cells appeared in increased proportions. An increased proportion of Leu-M1 positive cells were identified in the lymphocyte preparation from the patients, possibly reflecting the presence of activated granulocytes. Activation of the different cell types was studied with double staining technique. No activated Leu-3a+ or Leu-2a+ lymphocytes were present in blood when the patients were analyzed as one group, but when divided into subgroups according to inflammatory activity, the highest levels of activated Leu-2a+ lymphocytes were found in the group with active disease. Functional assays measuring DNA synthesis of T and B cells were normal. After three months treatment with sulphasalazine the patients showed clinical and laboratory improvement. The proportion of activated Leu-2a+ cells decreased during treatment, but no other changes occurred in the lymphocyte markers or lymphocyte functional tests. A patient control group showed no clinical improvement nor any changes in T cell markers. Our results support the concept that AS is a disease which affects the lymphocyte system and that the improvement induced by sulphasalazine may involve actions on this system.

Evidence for differential effects of sulphasalazine on systemic and mucosal immunity in rheumatoid arthritis.

“…Reductions in none, one, two or all three of the IgA, IgG, or IgM classes have been reported3 [49][50][51][52][53][54][55][56][57][58][59][60][61][62] Six of our patients had increased serum IgA anti-gliadin antibody levels. The serum levels of IgA anti-gliadin antibodies decreased significantly during SASP therapy.…”

Stimulation of whole blood cultures in patients with ankylosing spondylitis by a mitogen derived fromMycoplasma arthritidis (MAS) and other mitogens

“…There is strong evidence for the involvement of humoral and cell-mediated immunity in the pathogenesis of AS, though investigations on abnormalities in immune cell numbers in peripheral blood [15][16][17], cytokine production [7,8,18] and occurrence of certain antibodies to different microbes [2,19,20] show conflicting results. It should be considered that there is a wide diversity of presenting symptoms in AS, and clinical expression varies a lot [21].…”

No evidence of a genetic causal relationship between ankylosing spondylitis and iron homeostasis: A two-sample Mendelian randomization study

“…A study using nuclear microprobe technology measured the cellular storage of iron in granulocytes and platelets of 29 patients with AS, and found high levels of iron in granulocytes and platelets (12). Another two studies of blood cells in patients with AS also found that iron accumulation was significant in granulocytes and platelets in patients with AS (13,14). A case-control study of 30 patients with AS and 147 age -and sex-matched healthy controls found that iron intake was higher in patients with AS and that iron accumulation was significant in patients with AS (15).…”