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Myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (EAE) is the most commonly used animal model of multiple sclerosis. However, variations in the induction protocol can affect EAE progression, and may reduce the comparability of data. In the present study, we investigated the influence of the different components used for EAE induction in C57BL/6J mice on disease progression. In the present study, MOG 35–55 -induced chronic EAE in C57BL/6J mice has been applied as a model to challenge optimal pertussis toxin (PTx) dosing, while considering variations in batch potency. We demonstrate that the dosage of PTx, adjusted to its potency, influences EAE development in a dose-dependent manner. Our data show that with our protocol, which considers PTx potency, C57BL/6J mice consistently develop symptoms of EAE. The mice show a typical chronic course with symptom onset after 10.5 ± 1.08 days and maximum severity around day 16 postimmunization followed by a mild remission of symptoms. Previously studies reveal that alterations in PTx dosing directly modify EAE progression. Our present study highlights that PTx batches differ in potency, resulting in inconsistent EAE induction. We also provide a clear protocol that allows a reduction in the number of mice used in EAE experiments, while maintaining consistent results. Higher standards for comparability and reproducibility are needed to ensure and maximize the generation of reliable EAE data. Specifically, consideration of PTx potency. With our method of establishing consistent EAE pathogenesis, improved animal welfare standards and a reduction of mice used in experimentation can be achieved. • Pertussis toxin lots may vary in its potency, influencing the pathogenesis of EAE. • We titrated pertussis toxin to an optimal dose for a consistent EAE induction. • We provide a reliable protocol to achieve a higher degree of comparability. • This protocol helps to reduce the number of mice used in preclinical research. [ABSTRACT FROM AUTHOR]

Glioblastoma (GBM) is an aggressive and devastating primary brain cancer which responds very poorly to treatment. The average survival time of patients is only 14–15 months from diagnosis so there is a clear and unmet need for the development of novel targeted therapies to improve patient outcomes. The multifunctional cytokine TGFβ plays fundamental roles in development, adult tissue homeostasis, tissue wound repair and immune responses. Dysfunction of TGFβ signalling has been implicated in both the development and progression of many tumour types including GBM, thereby potentially providing an actionable target for its treatment. This review will examine TGFβ signalling mechanisms and their role in the development and progression of GBM. The targeting of TGFβ signalling using a variety of approaches including the TGFβ binding protein Decorin will be highlighted as attractive therapeutic strategies. • TGFβ can act as a context dependent tumour suppressor and tumour promoter in GBM. • TGFβ can modulate GBM tumour cell proliferation, migration, invasion and stemness. • TGFβ can modulate the tumour microenvironment in GBM. • TGFβ signalling is a promising target for therapeutic intervention for some GBM. • DCN may have therapeutic potential in GBM. [ABSTRACT FROM AUTHOR]