Publications by authors named "M Gadina"
Cytokines function as communication tools of the immune system, serving critical functions in many biological responses and shaping the immune response. When cytokine production or their biological activity goes awry, the homeostatic balance of the immune response is altered, leading to the development of several pathologies such as autoimmune and inflammatory disorders. Cytokines bind to specific receptors on cells, triggering the activation of intracellular enzymes known as Janus kinases (JAKs).
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- - Systemic lupus erythematosus (SLE) heightens cardiovascular disease (CVD) risk in patients, and traditional risk factors alone do not account for this increased risk, prompting a need for identifying specific blood immunologic signatures that may help pinpoint at-risk subgroups.
- - A study involving 77 SLE patients and 27 healthy controls assessed cardiovascular metrics like arterial stiffness and coronary plaque through advanced imaging techniques, along with blood analysis via RNA sequencing and inflammatory protein quantification.
- - Results showed higher CAVI, TBR, and noncalcified coronary plaque in SLE patients compared to controls, with specific immune-related genes and serum proteins identified as correlated with increased cardiovascular risk, indicating disrupted immune and metabolic pathways
Article Synopsis
- The linear ubiquitin assembly complex (LUBAC), made up of HOIP, HOIL-1, and SHARPIN, is crucial for immune responses, with deficiencies leading to severe issues like immunodeficiency and autoinflammation.
- Two individuals with SHARPIN deficiency exhibited autoinflammatory symptoms but did not have the expected skin problems seen in other cases, and their cells showed reduced immune responses.
- Treatment with anti-TNF therapies successfully resolved the autoinflammatory symptoms in one case, highlighting LUBAC's important role in managing immune cell death and maintaining immune balance in humans.
Objectives: To study the molecular pathogenesis of PAPA (pyogenic arthritis, pyoderma gangrenosum and acne) syndrome, a debilitating hereditary autoinflammatory disease caused by dominant mutation in .
Methods: Gene knock-out and knock-in mice were generated to develop an animal model. THP1 and retrovirally transduced U937 human myeloid leukaemia cell lines, peripheral blood mononuclear cells, small interfering RNA (siRNA) knock-down, site-directed mutagenesis, cytokine immunoassays, coimmunoprecipitation and immunoblotting were used to study inflammasome activation.