BLyS and April serum levels in patients with autoimmune thyroid diseases

Fabris, Martina; Grimaldi, Franco; Villalta, Danilo; Picierno, Alessia; Fabro, Cinzia; Bolzan, M.; Vita, Salvatore De; Tonutti, Elio

doi:10.1016/j.autrev.2009.07.005

Cited by 29 publications

(21 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This fi nding suggested that IL-16, like IL-2 receptors [ 26 ] , may be involved in autoantibody reactions in the thyroid. Serum IL-16 and RANTES concentrations are not correlated with the levels of pathognomonic auto-antibodies, TPOAb and TGAb, suggesting that these cytokines are not quantitatively related to B-cell secretion in HT [ 25 ] . These results are in accordance with the evidence that TPOAb and TgAb do not correlate with disease activity and may not have a predominant pathogenic role; they are frequently discovered in other autoimmune conditions and in healthy people but not in clinically evident autoimmune thyroiditis [ 25 , 27 ] .…”

mentioning

confidence: 71%

“…To identify the infl uence of thyroid hormone on cytokine expression, we analyzed the serum cytokines in HT patients treated with or without L -thyroxine therapy. Of note, patients undergoing L -thyroxine therapy may present transient or persistent states of hyperthyroidism, resembling the condition of GD patients [ 25 ] . We found that levels of IL-16 and RANTES in HT patients were comparable, regardless of whether thyroid function was hyperthyroid or euthyroid following L -thyroxine therapy or hypothyroid before therapy.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Elevated Serum IL-16 and RANTES Levels in Patients with Autoimmune Thyroid Diseases and Modulation by Methimazole Therapy

Zheng

Chen

et al. 2012

Horm Metab Res

View full text Add to dashboard Cite

Interleukine-16 (IL-16) and RANTES (regulated upon activation, normal T cell expressed and secreted) are 2 cytokines with the function of T helper cell recruitment, which might play a key role in pathogenesis of autoimmune thyroid diseases (AITD). This study was aimed to evaluate the IL-16 and RANTES in patients with AITD. Serum IL-16 and RANTES levels were measured in patients with Graves' disease (GD; n=45), Hashimoto's thyroiditis (HT; n=68), nontoxic multinodular goiter (NTMNG; n=20), and healthy individuals (n=61). The results showed that serum IL-16 and RANTES levels were elevated both in HT and higher in untreated GD patients when compared to NTMNG patients and the healthy individuals, which were decreased after MMI therapy in untreated GD patients. However, in HT patients, serum IL-16 and RANTES levels were comparable among the conditions of hyperthyroid and euthyroid received by l-thyroxine therapy and untreated hypothyroid. Furthermore, serum IL-16 levels were correlated with FT3, FT4, TRAb in GD, but not in HT patients. The data did not show any correlation between RANTES levels and clinical factors. In conclusion, IL-16 and RANTES might be involved in the pathogenesis of GD and HT, and serum IL-16 levels in GD maybe a potential marker of disease activity and severity.

show abstract

mentioning

confidence: 71%

mentioning

confidence: 99%

Elevated Serum IL-16 and RANTES Levels in Patients with Autoimmune Thyroid Diseases and Modulation by Methimazole Therapy

Zheng

Chen

et al. 2012

Horm Metab Res

View full text Add to dashboard Cite

show abstract

“…This cytokine plays a key role in the development of diabetes in NOD mice [45, 46], and previous studies have reported increased serum levels of BAFF in individuals with autoimmune thyroid diseases [47] and rheumatoid arthritis [48]. Decreased expression of the BAFF receptor has also been reported on B cells in children with type 1 diabetes [15].…”

Section: Discussionmentioning

confidence: 99%

Loss of CXCR3 expression on memory B cells in individuals with long-standing type 1 diabetes

et al. 2018

View full text Add to dashboard Cite

Aims/hypothesisIslet-specific autoantibodies can predict the development of type 1 diabetes. However, it remains unclear if B cells, per se, contribute to the causal pancreatic immunopathology. We aimed to identify phenotypic signatures of disease progression among naive and memory B cell subsets in the peripheral blood of individuals with type 1 diabetes.MethodsA total of 69 participants were recruited across two separate cohorts, one for discovery purposes and the other for validation purposes. Each cohort comprised two groups of individuals with type 1 diabetes (one with newly diagnosed type 1 diabetes and the other with long-standing type 1 diabetes) and one group of age- and sex-matched healthy donors. The phenotypic characteristics of circulating naive and memory B cells were investigated using polychromatic flow cytometry, and serum concentrations of various chemokines and cytokines were measured using immunoassays.ResultsA disease-linked phenotype was detected in individuals with long-standing type 1 diabetes, characterised by reduced C-X-C motif chemokine receptor 3 (CXCR3) expression on switched (CD27+IgD−) and unswitched (CD27intermediateIgD+) memory B cells. These changes were associated with raised serum concentrations of B cell activating factor and of the CXCR3 ligands, chemokine (C-X-C motif) ligand (CXCL)10 and CXCL11. A concomitant reduction in CXCR3 expression was also identified on T cells.Conclusions/interpretationOur data reveal a statistically robust set of abnormalities that indicate an association between type 1 diabetes and long-term dysregulation of a chemokine ligand/receptor system that controls B cell migration.Electronic supplementary materialThe online version of this article (10.1007/s00125-018-4651-x) contains peer-reviewed but unedited supplementary material, which is available to authorised users.

show abstract

“…This is distinct from other autoimmune-prone mouse models, including NZB, (NZB 3 NZW)F 1 , MRL-lpr, and BAFF-Tg mouse strains, in which MZ B cell expansion is governed by extrinsic factors such as BAFF overproduction (6)(7)(8)(9). In humans, aberrant pathogenic activity by MZ B cells in Sjö gren's syndrome and Grave's disease has also been associated with elevated levels of systemic BAFF (10,11,60,61). However, given that not all patients with these diseases exhibit elevated levels of BAFF, it is possible that irregularities in pathways regulating movement of B cells could constitute another mechanism that leads to expansion and pathogenic activity of the MZ subset.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic Molecular Factors Cause Aberrant Expansion of the Splenic Marginal Zone B Cell Population in Nonobese Diabetic Mice

Stolp

Mariño

Batten

et al. 2013

The Journal of Immunology

View full text Add to dashboard Cite

Marginal zone (MZ) B cells are an innate-like population that oscillates between MZ and follicular areas of the splenic white pulp. Differentiation of B cells into the MZ subset is governed by BCR signal strength and specificity, NF-κB activation through the B cell–activating factor belonging to the TNF family (BAFF) receptor, Notch2 signaling, and migration signals mediated by chemokine, integrin, and sphingosine-1-phosphate receptors. An imbalance in splenic B cell development resulting in expansion of the MZ subset has been associated with autoimmune pathogenesis in various murine models. One example is the NOD inbred mouse strain, in which MZ B cell expansion has been linked to development of type 1 diabetes and Sjögren’s syndrome. However, the cause of MZ B cell expansion in this strain remains poorly understood. We have determined that increased MZ B cell development in NOD mice is independent of T cell autoimmunity, BCR specificity, BCR signal strength, and increased exposure to BAFF. Rather, mixed bone marrow chimeras showed that the factor(s) responsible for expansion of the NOD MZ subset is B cell intrinsic. Analysis of microarray expression data indicated that NOD MZ and precursor transitional 2-MZ subsets were particularly dysregulated for genes controlling cellular trafficking, including Apoe, Ccbp2, Cxcr7, Lgals1, Pla2g7, Rgs13, S1pr3, Spn, Bid, Cd55, Prf1, and Tlr3. Furthermore, these B cell subsets exhibited an increased steady state dwell time within splenic MZ areas. Our data therefore reveal that precursors of mature B cells in NOD mice exhibit an altered migration set point, allowing increased occupation of the MZ, a niche favoring MZ B cell differentiation.

show abstract

BLyS and April serum levels in patients with autoimmune thyroid diseases

Cited by 29 publications

References 39 publications

Elevated Serum IL-16 and RANTES Levels in Patients with Autoimmune Thyroid Diseases and Modulation by Methimazole Therapy

Elevated Serum IL-16 and RANTES Levels in Patients with Autoimmune Thyroid Diseases and Modulation by Methimazole Therapy

Loss of CXCR3 expression on memory B cells in individuals with long-standing type 1 diabetes

Intrinsic Molecular Factors Cause Aberrant Expansion of the Splenic Marginal Zone B Cell Population in Nonobese Diabetic Mice

Contact Info

Product

Resources

About