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Takasugi, Koji; Yamamura, Masatoshi; Iwahashi, Mitsuhiro; Otsuka, Fumio; Yamana, Jiro; Sunahori, Katsue; Kawashima, Masanori; Yamada, Masao; Makino, Hírofumi

doi:10.1186/ar2015

Cited by 19 publications

(8 citation statements)

References 40 publications

(52 reference statements)

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“…Purkinje cells express receptors for both GM-CSF [67] and M-CSF [68], thus it is possible that altered levels of these two growth factors influence the maturation of the Purkinje cells, leading to language impairment. Notably, IL-10 is known to inhibit the action of GM-CSF [69], and also to act in synergy with M-CSF [70], thus, its involvement in non-verbal ASD, together with that of GM-CSF and M-CSF, seems highly conceivable.…”

Section: Discussionmentioning

confidence: 99%

Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder

Napolioni

Ober-Reynolds

Szelinger

et al. 2013

J Neuroinflammation

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ObjectiveConverging lines of evidence point to the existence of immune dysfunction in autism spectrum disorder (ASD), which could directly affect several key neurodevelopmental processes. Previous studies have shown higher cytokine levels in patients with autism compared with matched controls or subjects with other developmental disorders. In the current study, we used plasma-cytokine profiling for 25 discordant sibling pairs to evaluate whether these alterations occur within families with ASD.MethodsPlasma-cytokine profiling was conducted using an array-based multiplex sandwich ELISA for simultaneous quantitative measurement of 40 unique targets. We also analyzed the correlations between cytokine levels and clinically relevant quantitative traits (Vineland Adaptive Behavior Scale in Autism (VABS) composite score, Social Responsiveness Scale (SRS) total T score, head circumference, and full intelligence quotient (IQ)). In addition, because of the high phenotypic heterogeneity of ASD, we defined four subgroups of subjects (those who were non-verbal, those with gastrointestinal issues, those with regressive autism, and those with a history of allergies), which encompass common and/or recurrent endophenotypes in ASD, and tested the cytokine levels in each group.ResultsNone of the measured parameters showed significant differences between children with ASD and their related typically developing siblings. However, specific target levels did correlate with quantitative clinical traits, and these were significantly different when the ASD subgroups were analyzed. It is notable that these differences seem to be attributable to a predisposing immunogenetic background, as no other significant differences were noticed between discordant sibling pairs. Interleukin-1β appears to be the cytokine most involved in quantitative traits and clinical subgroups of ASD.ConclusionsIn the present study, we found a lack of significant differences in plasma-cytokine levels between children with ASD and in their related non-autistic siblings. Thus, our results support the evidence that the immune profiles of children with autism do not differ from their typically developing siblings. However, the significant association of cytokine levels with the quantitative traits and the clinical subgroups analyzed suggests that altered immune responses may affect core feature of ASD.

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Section: Discussionmentioning

confidence: 99%

Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder

Napolioni

Ober-Reynolds

Szelinger

et al. 2013

J Neuroinflammation

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“…Visualizing the antibody-antigen interaction can be accomplished by immunoperoxidase staining (an antibody is conjugated to peroxidase that can catalyze a color-producing reaction) [38] or immunofluorescence (the antibody is tagged to a fluorescein) [40]. In comparison with such a semiquantitative method, flow cytometry analysis has the advantage to evaluate quantitatively the receptor expression and to gain novel insights into the TNF-mediated pathophysiology of kidney diseases using monoclonal TNFR antibodies [21,41,42,43]. The utility of spectral variants of green fluorescent protein in flow cytometric fluorescence resonance energy transfer analysis of TNFRs has been demonstrated.…”

Section: Methodsmentioning

confidence: 99%

Tumor Necrosis Factor Receptors: Biology and Therapeutic Potential in Kidney Diseases

Speeckaert

Laute³

et al. 2012

Am J Nephrol

104

101

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The major evolutionary advance represented in the human immune system is a mechanism of antigen-directed immunity in which tumor necrosis factor (TNF)-α and TNF receptors (TNFRs) play essential roles. Binding of TNF-α to the 55-kDa type I TNFR (TNFR1, TNFRSF1A, CD120a, p55) or the 75-kDa type II TNFR (TNFR2, TNFRSF1B, CD120b, p75) activates signaling pathways controlling inflammatory, immune and stress responses, as well as host defense and apoptosis. Multiple studies have investigated the role of TNFRs in the development of early and late renal failure (diabetic nephropathy, nephroangiosclerosis, acute kidney transplant rejection, renal cell carcinoma, glomerulonephritis, sepsis and obstructive renal injury). This article reviews the general characteristics, the analytical aspects and the biology of TNFRs in this domain. In addition, the potential therapeutic application of specific TNFR blockers is discussed.

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“…Considering the fact that TNFR2 expression has repeatedly been linked to IL-10 production ( 48 , 49 ), this seemed an attractive hypothesis. However, while data from mice demonstrated a role of TNFR2 in B cell activation ( 50 ), in human B cells only scarce information was available.…”

Section: Introductionmentioning

confidence: 99%

Expression of Tumor Necrosis Factor Receptor 2 Characterizes TLR9-Driven Formation of Interleukin-10-Producing B Cells

et al. 2018

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B cell-derived interleukin-10 (IL-10) production has been described as a hallmark for regulatory function in B lymphocytes. However, there is an ongoing debate on the origin of IL-10-secreting B cells and lack of specific surface markers has turned into an important obstacle for studying human B regulatory cells. In this study, we propose that tumor necrosis factor receptor 2 (TNFR2) expression can be used for enrichment of IL-10-secreting B cells. Our data confirm that IL-10 production can be induced by TLR9 stimulation with CpG ODN and that IL-10 secretion accompanies differentiation of peripheral blood B cells into plasma blasts. We further show that CpG ODN stimulation induces TNFR2 expression, which correlates with IL-10 secretion and terminal differentiation. Indeed, flow cytometric sorting of TNFR2+ B cells revealed that TNFR2+ and TNFR2− fractions correspond to IL-10+ and IL-10− fractions, respectively. Furthermore, CpG-induced TNFR2+ B cells were predominantly found in the IgM+ CD27+ B cell subset and spontaneously released immunoglobulin. Finally, our data corroborate the functional impact of TNFR2 by demonstrating that stimulation with a TNFR2 agonist significantly augments IL-10 and IL-6 production in B cells. Altogether, our data highlight a new role for TNFR2 in IL-10-secreting human B lymphocytes along with the potential to exploit this finding for sorting and isolation of this currently ill-defined B cell subset.

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Abstract: Despite its potent ability to inhibit proinflammatory cytokine synthesis, interleukin (IL

Cited by 19 publications

References 40 publications

Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder

Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder

Tumor Necrosis Factor Receptors: Biology and Therapeutic Potential in Kidney Diseases

Expression of Tumor Necrosis Factor Receptor 2 Characterizes TLR9-Driven Formation of Interleukin-10-Producing B Cells

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