Publications by authors named "Natalie Gross"
(1) Background: Autoimmune pancreatitis (AIP) is mainly treated with steroids. Using an AIP mouse model, we investigated two potential alternatives, the transforming growth factor-β-activated kinase 1 inhibitor, takinib, and the Janus kinase inhibitor, tofacitinib. (2) Methods: In a multicenter preclinical study, MRL/MpJ mice were injected with polyinosinic/polycytidylic acid (poly I:C) for two weeks to induce AIP.
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- A balanced immune system is crucial for defending against infections and preventing autoimmune diseases; an ineffective response allows infections to thrive, while uncontrolled activation can cause inflammatory disorders.
- Researchers screened 1200 small molecules to find drugs that can modify immune cell functions, focusing on T cells, B cells, and polymorphonuclear leukocytes (PMNs) for chronic inflammatory diseases.
- They identified candidate drugs like pyrvinium pamoate, which effectively suppressed B cell activation and slowed down an autoimmune condition, and studied mechanisms in gene-deleted mice to further understand how these actions occur, paving the way for potential drug repurposing to manage immune responses.
Article Synopsis
- - Epidermolysis bullosa acquisita (EBA) is an autoimmune skin disease caused by autoantibodies against type VII collagen, making its treatment challenging with a long median remission time of 9 months.
- - Research shows that removing regulatory T cells increases inflammation and blistering in EBA models, and the role of interferon gamma (IFN-γ) in this process was previously unclear.
- - Treatment with an anti-IFN-γ antibody resulted in significant clinical improvement of EBA symptoms and reduced inflammation, suggesting that targeting IFN-γ could be a viable therapeutic approach for EBA and similar conditions.
Article Synopsis
- - Psoriasis is a chronic skin condition, and Aldara® (imiquimod) cream applied to mice creates a model (AIPD) to study the disease's development and severity arising from genetic differences in 13 inbred mouse strains.
- - The research identified that variations in the Itga11 gene, which encodes a protein involved in skin inflammation and wound healing, are linked to different severities of AIPD among the mouse strains.
- - Mice lacking the Itga11 gene showed reduced inflammation and fewer immune cells in their skin when AIPD was induced, suggesting that Itga11 is crucial for the inflammatory responses in psoriasis and could be a potential target for new treatments.
Chronic blistering at the skin and/or mucous membranes, accompanied by a varying degree of inflammation, is the clinical hallmark of pemphigoid diseases that impose a major medical burden. Pemphigoid diseases are caused by autoantibodies targeting structural proteins of the epithelial basement membrane. One major pathogenic pathway of skin blistering and inflammation is activation of myeloid cells following Fc gamma receptor-dependent binding to the skin-bound immune complexes.
View Article and Find Full Text PDFInvestigating atherosclerosis and endothelial dysfunction has mainly become established in genetically modified ApoE or LDL-R mice transgenic models. A new AAV-PCSK9DY mouse model with no genetic modification has now been reported as an alternative atherosclerosis model. Here, we aimed to employ this AAV-PCSK9 mouse model to quantify the mechanical stiffness of the endothelial surface, an accepted hallmark for endothelial dysfunction and forerunner for atherosclerosis.
View Article and Find Full Text PDFClass I phosphoinositide 3-kinases (PI3K) have been implemented in pathogenesis of experimental epidermolysis bullosa acquisita (EBA), an autoimmune skin disease caused by type VII collagen (COL7) autoantibodies. Mechanistically, inhibition of specific PI3K isoforms, namely PI3Kβ or PI3Kδ, impaired immune complex (IC)-induced neutrophil activation, a key prerequisite for EBA pathogenesis. Data unrelated to EBA showed that neutrophil activation is also modulated by PI3Kα and γ, but their impact on the EBA has, so far, remained elusive.
View Article and Find Full Text PDFRegulatory T (Treg) cells induce immunologic tolerance by suppressing effector functions of conventional lymphocytes in the periphery. On the other hand, immune silencing is mediated by recognition of phosphatidylserine (PS) on apoptotic cells by phagocytes. Here we describe expression of the PS-binding protein Annexin V (ANXA5) in CD4 CD25 Treg cells at the mRNA and protein levels.
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