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The complement system plays a major role in the autoimmune disease, systemic lupus erythematosus (SLE). This review highlights the many roles of complement for
One explanation for the high burden of allergic and autoimmune diseases in industrialized countries is inappropriate immune development under modern...
A hallmark of atopic asthma is development of chronic airways hyper-responsiveness (AHR) that persists in the face of ongoing exposure to perennial...
Information is accumulating which implicates airway inflammation resulting from respiratory viral infections, acting against a background of atopy.
Nanoparticles are being developed for diverse biomedical applications, but there is concern about potential to promote inflammation, particularly in the lungs.
Asthma is a chronic disease of the airways, most commonly driven by immuno-inflammatory responses to ubiquitous airborne antigens.
The hallmark of atopic asthma is transient airways hyperresponsiveness (AHR) preceded by aeroallergen-induced Th-cell activation.
Multiple sclerosis (MS) is an immune-mediated inflammatory disease of the central nervous system that results in demyelination of axons, inefficient signal transmission and reduced muscular mobility. Recent findings suggest that B cells play a significant role in disease development and pathology. To further explore this, B cell profiles in peripheral blood from 28 treatment-naive patients with early MS were assessed using flow cytometry and compared to 17 healthy controls.
The immunological mechanisms that contribute to multiple sclerosis (MS) differ between males and females. Females are 2-3 times more likely to develop MS compared to males, however the reason for this discrepancy is unknown. Once MS is established, there is a more inflammatory yet milder form of disease in females whereas males generally suffer from more severe disease and faster progression, neural degradation, and disability.
Asthma is a chronic inflammatory disease of the small and large conducting airway mucosa characterised by Th2 cell immunity.