Polyclonal B cell activation in ankylosing spondylitis.

Barbieri, Paola; Olivieri, Ignazio; Benedettini, G; Marelli, P; Ciompi, M.L.; Pasero, G; Campa, Michael J.

doi:10.1136/ard.49.6.396

Cited by 5 publications

(3 citation statements)

References 17 publications

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“…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].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 1997

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In this study we compared cytokine production and cell proliferation of immunocompetent cells derived from patients with ankylosing spondylitis (AS) to those from healthy blood donors using a whole blood assay. To this end, blood cell cultures were stimulated with the superantigens MAS (Mycoplasma arthritidis supernatant) and staphylococcal enterotoxin B (SEB) and the plant lectins phytohaemagglutinin (PHA) and concanavalin A (Con A). The number of white blood cells (WBC) and lymphocyte subsets were also determined. Cell proliferation and levels of interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) were measured after stimulation with the different mitogens. An ELISA test was used to analyse supernatant cytokine levels. Individuals with AS showed significantly lower IFN-gamma concentrations and markedly lower cell proliferation rates with all tested mitogens than healthy controls, while there was no significant difference in IL-6 synthesis. IL-1 beta levels were slightly impaired in the patient group, but only blood cell cultures stimulates with MAS showed a statistical significance. Furthermore, there was a significant elevation of leucocytes and lymphocytes in patients with AS resulting in higher numbers of CD4-positive cells, which implies a higher CD4:CD8 cell ratio. CD19- and CD8-positive cells were not significantly distinct compared to healthy controls. This deviation in cytokine levels and cell proliferation points to a suppression of T lymphocytes. A disturbed T-lymphocyte function may play a part in the pathogenesis of AS.

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Section: Discussionmentioning

confidence: 99%

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

et al. 1997

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“…It has been previously reported that neutrophils are more active in AS patients [ 26 ] but no differences in total B or T cell numbers were reported [ 27 ]. In our study no differences were found in the frequency of granulocytes and T and B cells between any of the studied groups.…”

Section: Discussionmentioning

confidence: 99%

Effect of Tumor Necrosis Factor Inhibitor Therapy on Osteoclasts Precursors in Ankylosing Spondylitis

et al. 2015

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IntroductionAnkylosing Spondylitis (AS) is characterized by excessive local bone formation and concomitant systemic bone loss. Tumor necrosis factor (TNF) plays a central role in the inflammation of axial skeleton and enthesis of AS patients. Despite reduction of inflammation and systemic bone loss, AS patients treated with TNF inhibitors (TNFi) have ongoing local bone formation. The aim of this study was to assess the effect of TNFi in the differentiation and activity of osteoclasts (OC) in AS patients.Methods13 AS patients treated with TNFi were analyzed at baseline and after a minimum follow-up period of 6 months. 25 healthy donors were recruited as controls. Blood samples were collected to assess receptor activator of nuclear factor kappa-B ligand (RANKL) surface expression on circulating leukocytes and frequency and phenotype of monocyte subpopulations. Quantification of serum levels of bone turnover markers and cytokines, in vitro OC differentiation assay and qRT-PCR for OC specific genes were performed.ResultsRANKL+ circulating lymphocytes (B and T cells) and IL-17A, IL-23 and TGF-β levels were decreased after TNFi treatment. We found no differences in the frequency of the different monocyte subpopulations, however, we found decreased expression of CCR2 and increased expression of CD62L after TNFi treatment. OC number was reduced in patients at baseline when compared to controls. OC specific gene expression was reduced in circulating OC precursors after TNFi treatment. However, when cultured in OC differentiating conditions, OC precursors from AS TNFi-treated patients showed increased activity as compared to baseline.ConclusionIn AS patients, TNFi treatment reduces systemic pro osteoclastogenic stimuli. However, OC precursors from AS patients exposed to TNFi therapy have increased in vitro activity in response to osteoclastogenic stimuli.

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“…Apart from Th17, other T cell subsets such as Th1 [14,17] and T follicular helper cell (Tfh) which is correlated with B cell subtypes [18][19][20] are also involved in the pathogenesis of AS. Besides, several studies confirm that B cells participate in the pathogenesis of AS, such as increasing regulatory B cell (Breg) in peripheral blood of AS [21][22][23][24]. Nevertheless, the impact of anti-TNF-α therapy on those immune cells in AS patients is still not clearly defined, and the impact of immune cells on treatment response is also largely elusive.…”

Section: Introductionmentioning

confidence: 99%

Immunological Changes in Peripheral Blood of Ankylosing Spondylitis Patients during Anti-TNF-α Therapy and Their Correlations with Treatment Outcomes

Chen

Qian

Yuan

et al. 2021

Journal of Immunology Research

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Tumor necrosis factor-α (TNF-α) inhibitors are the main types of biological conventional synthetic disease-modifying antirheumatic drugs and have efficacy in treating ankylosing spondylitis (AS) which is not sensitive for nonsteroidal anti-inflammatory drug. However, the impact of TNF-α inhibitors on immune cells in patients with AS is still clearly undefined, and the impact of immune cells on treatment response is also largely elusive. This study is aimed at evaluating the longitudinal changes of circulating immune cells after anti-TNF-α therapy and their associations with treatment response in AS patients. Thirty-five AS patients receiving the treatment of anti-TNF-α therapy were included into this prospective observational study. The frequencies of immune cells including Th1, Th2, Th17, regulatory T cell (Treg), T follicular helper cell (Tfh), and regulatory B cell (Breg) in the peripheral blood were measured by flow cytometry at baseline and 4 time points after therapy. The difference in the circulating immune cells between responders and nonresponders was compared. This study suggested that anti-TNF-α therapy could significantly reduce circulating proinflammatory immune cells such as Th17 and Tfh, but significantly increased the percentages of circulating Treg and Breg. Moreover, circulating Breg may be a promising predictor of response to anti-TNF-α therapy in AS patients.

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Polyclonal B cell activation in ankylosing spondylitis.

Cited by 5 publications

References 17 publications

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

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

Effect of Tumor Necrosis Factor Inhibitor Therapy on Osteoclasts Precursors in Ankylosing Spondylitis

Immunological Changes in Peripheral Blood of Ankylosing Spondylitis Patients during Anti-TNF-α Therapy and Their Correlations with Treatment Outcomes

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