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To show underlying mechanisms, we examined differences in T-cell gene expression in samples at birth and at 1 year in children with and without IgE allergy.
This methodology has significant potential to identify covert interactions between inflammatory pathways triggered by vaccination, and as such may be a...
Concerns about the risk of inducing immune deviation-associated "neonatal tolerance" as described in mice have restricted the widespread adoption...
Atopy and asthma are commonly initiated during early life, and there is increasing interest in the development of preventive treatments for at-risk children.
Alexander David Deborah Larcombe Martino Strickland BScEnv (Hons) PhD BSc PhD PhD Honorary Research Fellow Head, Chronic Diseases Research Head,
Cancer vaccination drives the generation of anti-tumor T cell immunity and can be enhanced by the inclusion of effective immune adjuvants such as type I interferons (IFNs). Whilst type I IFNs have been shown to promote cross-priming of T cells, the role of individual subtypes remains unclear. Here we systematically compared the capacity of distinct type I IFN subtypes to enhance T cell responses to a whole-cell vaccination strategy in a pre-clinical murine model.
The first few days of life are characterized by rapid external and internal changes that require substantial immune system adaptations. Despite growing evidence of the impact of this period on lifelong immune health, this period remains largely uncharted.
The absence of a diagnostic test for acute rheumatic fever (ARF) is a major impediment in managing this serious childhood condition. ARF is an autoimmune condition triggered by infection with group A Streptococcus.
Over the past 20 years natural killer (NK) cell-based immunotherapies have emerged as a safe and effective treatment option for patients with relapsed or refractory leukemia. Unlike T cell-based therapies, NK cells harbor an innate capacity to eliminate malignant cells without prior sensitization and can be adoptively transferred between individuals without the need for extensive HLA matching.
This protocol describes bilateral murine tumor models that display a symmetrical yet dichotomous response to immune checkpoint blockade