Febrile temperatures control antineutrophil cytoplasmic autoantibody–induced neutrophil activation via inhibition of phosphatidylinositol 3‐kinase/Akt

Vietinghoff, Sibylle von; Choi, Mira; Rolle, Susanne; Luft, Friedrich C.; Kettritz, Ralph

doi:10.1002/art.22832

Cited by 5 publications

(9 citation statements)

References 34 publications

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“…We observed two interesting effects of short fever‐like temperature spikes on neutrophils that could be clinically relevant in ANCA patients. Heat exposure abrogated PI3K/Akt activation and respiratory burst in primed neutrophils challenged by ANCA [66]. ANCA‐induced phosphorylation of p38 MAPK and ERK was not affected.…”

Section: Anca Activate Signalling Pathways and Neutrophil Functions Tmentioning

confidence: 92%

How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

Kettritz

2012

Clinical and Experimental Immunology

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SummaryNeutrophils are pivotal to host defence during infectious diseases. However, activated neutrophils may also cause undesired tissue damage. Ample examples include small-vessel inflammatory diseases (vasculitis) that are associated with anti-neutrophil cytoplasmic autoantibodies (ANCA) residing in the patients' plasma. In addition to being an important diagnostic tool, convincing evidence shows that ANCA are pathogenic. ANCA-neutrophil interactions induce important cellular responses that result in highly inflammatory necrotizing vascular damage. The interaction begins with ANCA binding to their target antigens on primed neutrophils, proceeds by recruiting transmembrane molecules to initiate intracellular signal transduction and culminates in activation of effector functions that ultimately mediate the tissue damage.

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Section: Anca Activate Signalling Pathways and Neutrophil Functions Tmentioning

confidence: 92%

How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

Kettritz

2012

Clinical and Experimental Immunology

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“…anti-neutrophil cytoplasmic autoantibodies) through NF-κBindependent signaling pathways as well. 15 On the other hand, fever-like temperatures were noted to activate NF-κB pathway in macrophages. 16 Fever range temperatures also induce T lymphocytes to produce stress proteins (such as heat-shock proteins-Hsp).…”

Section: Discussionmentioning

confidence: 99%

Transient positivity of anti-tissue transglutaminase IgA autoantibody in febrile children: a case-control study

et al. 2021

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Background. Fever is a physiological response activated by integrative interactions between the neuronal and immune systems. The association of fever with the development of autoantibodies against various self-antigens is controversial. We here evaluated if fever was associated with increased levels of anti-tissue transglutaminase (tTG) IgA autoreactive antibodies in children.Methods. This was a case-control study performed the Amir-Al-Momenin Hospital of Zabol City from January to December 2018. Febrile children (N=135) and apparently healthy counterparts (N=135) were included. Total IgA and anti-tTG IgA were measured by ELISA.Results. From 270 children evaluated, 144 (53.6%) and 126 (46.4%) were males and females, respectively. The mean age was 4.7 ± 2.6 years. The mean total IgA titer was 208 ± 100 mg/dl, and the mean anti-tTG IgA titer was 15.9 ± 68 mg/dl. There was a significant difference in the mean titer of anti-tTG IgA between apparently healthy controls (1.97 ± 1.12 mg/dl) and febrile children (30.2 ± 94.9 mg/dl, p=0.002). Positivity for anti-tTG IgA was observed in 16 (11.8%) out of 135 febrile children while no subject in the control group had positive results. One out of the 16 positive cases showed persistent elevated levels after fever disappearance. On biopsy examination, this child was confirmed to have celiac disease. Conclusions.We showed that fever can trigger the production of anti-tTG IgA autoantibody in children. It is recommended for pediatricians to be vigilant in interpreting anti-tTG IgA results during fever episodes and repeat positive cases after the cease of fever. It is also recommended to reassess anti-tTG IgA seropositivity in other clinical settings in future studies.

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“…Peripheral venous blood was drawn from healthy volunteers after local ethics board approval (MHH 2010/807) and informed consent. Neutrophilic granulocytes were isolated by density gradient centrifugation, as described previously .…”

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Pathogenetic role of glomerular CXCL13 expression in lupus nephritis

Worthmann

Gueler

Vietinghoff

et al. 2014

Clinical and Experimental Immunology

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SummaryPodocytes maintain the structure and function of the glomerular filtration barrier. However, podocytes have recently been implicated in the innate immune response, and their function as non-haematopoietic antigenpresenting cells was highlighted. We have shown previously that excessive expression of the chemokine CXCL13 is a distinctive early event for nephritis in a murine model of systemic lupus erythematosus (SLE). Furthermore, we found that CXCL13 is elevated significantly in the serum of patients with SLE-nephritis. In this study, we were able to show for the first time that (i) CXCL13 is expressed locally in glomeruli in a model for SLE-nephritis in mice and that (ii) incubation of human podocytes with CXCL13 induces receptor stimulation of CXCR5 with activation of signalling pathways, resulting in (iii) secretion of proinflammatory cytokines and chemokines in culture supernatant. This cytokine/chemokine cocktail can lead to (iv) a neutrophil respiratory burst in isolated human granulocytes. Taken together, our results provide further evidence that CXCL13 is involved in the pathogenesis of glomerulonephritis and that podocytes can play an active role in local proinflammatory immune responses. Thus, CXCL13 could be a direct target for the therapy of glomerulonephritis in general and for SLE-nephritis in particular.

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Febrile temperatures control antineutrophil cytoplasmic autoantibody–induced neutrophil activation via inhibition of phosphatidylinositol 3‐kinase/Akt

Cited by 5 publications

References 34 publications

How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

Transient positivity of anti-tissue transglutaminase IgA autoantibody in febrile children: a case-control study

Pathogenetic role of glomerular CXCL13 expression in lupus nephritis

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