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Airways hyperresponsiveness (AHR) is one of the major clinical features of allergic airways disease including allergic asthma
Head, Pregnancy and Early Life Immunology
Impaired interferon response and allergic sensitization may contribute to virus-induced wheeze and asthma development in young children. Plasmacytoid dendritic cells play a key role in antiviral immunity as critical producers of type I interferons.
The expression pattern of FcεRI on DC and basophils differentiates asthmatic from non-asthmatic atopic children
Our findings suggest that the proportion of degranulated basophils can also be associated with recurrent exacerbations
Allergic sensitization and reduced ability to respond to viral infections may contribute to virus-induced wheeze and asthma development in young children. Plasmacytoid dendritic cells (pDC) are rare immune cells that produce type I interferons (IFN-I) and play a key role in orchestrating immune responses against viruses.
The interaction of genetic and environmental contributions to immunological traits and their association with atopic disease remain unclear. Flow cytometry and in vitro cytokine responses were used to characterize immune profiles from 93 school-aged twin pairs. Using an established twin pair analytical strategy, the genetic and environmental influences on immunological traits were evaluated, along with their association with atopy. Our findings suggest strong genetic influence on several traits, particularly B cell abundance. In contrast, cytokine responses from in vitro stimulations appeared mainly shaped by environmental exposures.
IgE-mediated sensitisation to egg is common in infants. In some cases, the processes leading to egg sensitisation are established in early life, even before introduction to solid foods. The underlying mechanisms remain poorly understood.
Multiple sclerosis is associated with Epstein–Barr virus (EBV) infection, B-cell dysfunction, gut dysbiosis, and environmental and genetic risk factors, including female sex.
Tissue-resident memory T (TRM) cells have emerged as key players in the immune control of melanoma. These specialized cells are identified by expression of tissue retention markers such as CD69, CD103 and CD49a with downregulation of egress molecules such as Sphingosine-1-Phosphate Receptor-1 (S1PR1) and the lymphoid homing receptor, CD62L.