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https://www.selleckchem.com/products/lxh254.html Fibrotic diseases take a very heavy toll in terms of morbidity and mortality equal to or even greater than that caused by metastatic cancer. In this review, we examine the pathogenesis of fibrotic diseases, mainly addressing triggers for induction, processes that lead to progression, therapies and therapeutic trials. For the most part, we have focused on two fibrotic diseases with lung involvement, idiopathic pulmonary fibrosis, in which the contribution of inflammatory mechanisms may be secondary to non-immune triggers, and systemic sclerosis in which the contribution of adaptive immunity may be predominant. Staphylococcus aureus infections are common throughout the lifespan, with recurrent infections occuring in nearly half of infected children. There is no licensed vaccine, underscoring the need to better understand how S. aureus evades protective immunity. Despite much study, the relative contributions of antibodies and T cells to protection against S. aureus infections in humans are not fully understood. We prospectively quantified S. aureus-specific antibody levels by ELISA and T cell responses by ELISpot in S. aureus-infected and healthy children. S. aureus-specific antibody levels and T cell responses increased with age in healthy children, suggesting a coordinated development of anti-staphylococcal immunity. Antibody levels against leukotoxin E (LukE) and Panton-Valentine leukocidin (LukS-PV), but not α-hemolysin (Hla), were higher in younger infected children, compared with healthy children; these differences disappeared in older children. We observed a striking impairment of global and S. aureus-specific T cell function in children with invasive and non-invasive infection, suggesting that S. aureus-specific immune responses are dysregulated during childhood infection regardless of the infection phenotype. These findings identify a potential mechanism by which S. aureus infection actively evades adaptive imm

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