Serum levels of interleukin 1-?, tumor necrosis factor-?, soluble interleukin 2 receptor and soluble CD8 in seronegative spondylarthropathies

Abstract

Seronegative spondylarthropathies are disorders with the same predisposing antigen, namely HLA B27, a class I molecule of the HLA system. The mechanisms of the different diseases are unknown, and there is no proof of immune system participation. We have investigated patients with spondylarthropathies in order to search for an immunological component in the pathophysiology of these disorders, by measuring the serum level of two inflammatory cytokines--IL1 beta and TNF alpha--by a radioimmunological assay and the serum level of two soluble T cell activation markers--soluble IL2 receptor and soluble CD8--by an enzyme-linked immunosorbent assay. The choice of soluble CD8 can be explained by the strong link between HLA B27 and spondylarthropathies. Our series compared 24 patients to 24 healthy matched controls. A similar IL1 beta serum level was observed in both groups, while in the patients there was a nonsignificant increase in the TNF alpha level, a significant decrease in the soluble IL2 receptor level and a significant increase in the soluble CD8 serum level. The normal or moderately increased serum IL1 beta and TNF alpha levels in the disease group do not exclude a local role for these cytokines in the synovium or other inflammatory areas. However, we found a higher soluble CD8 serum level in the patient group. Most of these patients were in clinical exacerbation of their disease. As the serum level of soluble CD8 is well correlated with T CD8 lymphocyte activation, our data suggest that this lymphocyte subset is stimulated and consequently probably involved in seronegative spondylarthropathies.

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

“…Most studies have focused on T helper cytokines, consistently demonstrating an impaired IFN␥ signature in SpA T cells (27)(28)(29)(30). With regard to macrophage-derived mediators, only a limited number of studies have analyzed serum levels of proinflammatory cytokines in SpA, indicating an increase in IL-6 and TNF␣, but not IL-1␤, in SpA patients as compared with healthy controls (31)(32)(33). Of interest, this profile appeared to be more pronounced in patients with peripheral arthritis than in those with pure axial SpA (26).…”

Hypothalamic-pituitary-adrenal axis in patients with ankylosing spondylitis

“…3,6 A relationship has also been shown between disease activity in AS and IL-6, soluble interleukin 2 (IL-2) receptors and TNF-. 7,8 Endogenous glucocorticoids produced by the adrenal glands, under the control of the hypothalamus and pituitary, have an important role in the control of inflammation. It is now clear that the presence of inflammation, through the release of cytokines, constitutes a direct stimulus to the activity of the hypothalamus and pituitary, resulting in the production of adrenal glucocorticoids under the influence of ACTH.…”

Arterial stiffness indexes and serum cytokine levels in seronegative spondyloarthritis: relationships between stiffness markers and metabolic and immunoinflammatory variables

“…Several studies (12)(13)(14) have shown that TNF-α levels are raised at baseline in patients with SpA. Gratacos et al (15) showed that TNF-α and IL-6 levels were raised in patients with AS compared with patients with non-inflammatory back pain.…”