Publications by authors named "I Tindemans"

Article Synopsis
  • CD4 memory T cell reactivation is linked to chronic inflammatory bowel disease (IBD), affecting conditions like Crohn's disease (CD) and ulcerative colitis, with unclear differences in T cell regulation among patients.
  • In a study of pediatric IBD patients, a specific subgroup of therapy-naïve CD patients showed higher frequencies of a particular inflammatory T cell type (TIGITCD38T) associated with severe disease and elevated IFN-γ levels.
  • The research identified IL-12 as a key driver of this inflammatory response, with increased IL-12 signaling linked to the transformation of T cells into more pathogenic forms, correlating with worsened intestinal inflammation.
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Background: Despite its efficacy, rational guidance for starting/stopping first-line biologic treatment in individual paediatric Crohn's disease [CD] patients is needed. We assessed how serum immune profiles before and after first-line infliximab [FL-IFX] or conventional [CONV] induction therapy associate with disease remission at week 52.

Methods: Pre- [n = 86], and 10-14-week post-treatment [n = 84] sera were collected from patients with moderate-to-severe paediatric CD in the TISKids trial, randomized to FL-IFX [n = 48; five 5-mg/kg infusions over 22 weeks] or CONV [n = 43; exclusive enteral nutrition or oral prednisolone]; both groups received azathioprine maintenance.

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Introduction: Patients with paediatric-onset inflammatory bowel disease (PIBD) may develop a complicated disease course, including growth failure, bowel resection at young age and treatment-related adverse events, all of which can have significant and lasting effects on the patient's development and quality of life. Unfortunately, we are still not able to fully explain the heterogeneity between patients and their disease course and predict which patients will respond to certain therapies or are most at risk of developing a more complicated disease course. To investigate this, large prospective studies with long-term follow-up are needed.

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Allergic asthma is mediated by Th2 responses to inhaled allergens. Although previous experiments indicated that Notch signaling activates expression of the key Th2 transcription factor Gata3, it remains controversial how Notch promotes allergic airway inflammation. Here we show that T cell-specific Notch deficiency in mice prevented house dust mite-driven eosinophilic airway inflammation and significantly reduced Th2 cytokine production, serum IgE levels, and airway hyperreactivity.

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