Immunobiology
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread worldwide causing a pandemic with millions of infected people and deaths. Currently, the scientific community is working hard to develop a specific vaccine or treatment. However, since antibody production is an important part of the adaptive immune response, to develop vaccines and therapies, we must understand the antibody response to SARS-CoV-2 infection. In this work, we summarize the most important findings of antibody-mediated immunity against SARS-CoV-2 and highlight its role in the efficient use of plasma from convalescent patients and the direct application of antibodies as treatment.
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The complement system plays a key role in host-defense against common pathogens but must be tightly controlled to avoid inflammation and tissue damage. Polymorphisms in genes encoding two important negative regulators of the alternative complement pathway, complement factor H (CFH) and complement factor I (CFI), are associated with the risk for Age-Related Macular Degeneration (AMD), a leading cause of vision impairment in the ageing population. In this review, we will discuss the genetic basis of AMD and the potential impact of complement de-regulation on disease pathogenesis. Finally, we will highlight recent therapeutic approaches aimed at controlling complement activation in patients with AMD.
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Haemolytic uraemic syndrome (HUS) accounts for the most common cause of childhood acute renal failure. Characterized by the classical triad of a microangiopathic haemolytic anaemia, thrombocytopaenia and acute renal failure, HUS occurs as a result of Shiga-toxin producing microbes in 90% of cases. ⋯ With the advent of improved genetic diagnosis, it is likely that certain cases of infection-induced HUS may be attributed to underlying defects in complement components. This review summarises the interplay between complement and infection in the pathogenesis of HUS.
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A review of 250 patients with the catastrophic antiphospholipid (Asherson's) syndrome (CAPS) taken from the web site organized by the Europhospholipid Group (http://www.med.ub.es/MIMMUN/FORUM/CAPS. HTM) is presented in this paper. A short historical overview of the antiphospholipid syndrome (APS) is followed by a description of the "triggering" factors, associated autoimmune diseases, clinical presentation, presumed pathogenesis, prognosis, mode of death and suggested therapies. ⋯ Treatment may have to be continued for several weeks. Parenteral antibiotics may be indicated where an underlying infection is suspected. Antifungal therapy may also be indicated with prolonged treatment and the use of the monoclonal anti-CD20 molecule, Rituximab, has proven useful in those patients where thrombocytopenia poses a major risk of hemorrhage.
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Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. ⋯ Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte endothelial cell-cell interaction was strikingly reduced in the reperfused tissues as afflection of anti-inflammatory effect.