Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early childhood is a period of heightened susceptibility to infection due to immaturity of the immune system, and the nature of these developmental deficiencies is only partially understood. In this study, we focused on the ontogeny of the innate immune system by investigating the capacity of mononuclear cells to secrete a wide spectrum of inflammatory cytokines in response to interferon (IFN)-gamma priming and lipopolysaccharide (LPS) stimulation, namely IL-6, IL-10, IL-12, IL-18, IL-23, tumor necrosis factor (TNF)-alpha, and myxovirus resistance protein A, induced by type-I IFN, at several time points between birth (cord blood) and adulthood. Competence to produce all these cytokines followed a similar developmental pattern, with slow postnatal up-regulation from the response observed in cord blood. Unexpectedly, IL-6, IL-10, TNF-alpha, and IFN-gamma showed slow postnatal up-regulation but also elevated cord blood responses equal to or greater than the adult level. This was transient and not observed at 2 mo of age, and was not related to predelivery stress of the newborns. Variations in Toll-like receptor (TLR)4 function may account for these age related differences in cytokine responses, as TLR4 expression on neonatal monocytes post LPS stimulation was elevated and sustained relative to infants and adults.
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PMID:Postnatal development of monocyte cytokine responses to bacterial lipopolysaccharide. 1780 7

Trigger and risk factors in asthma are multiple, the most relevant at the time are: genetic, infectious (viral, bacterial, fungi and parasites), environmental (allergens, smoking, irritants, pollutants of cars, industries, work environment, etc.) and obesity. Asthma severity meets influenced by the age, sex, pregnancy, immunological system immaturity and the atopic march. The pathogeny of the inflammatory allergic process more than an imbalance Th1/Th2, mast cells, eosinophils and IgE, today includes the important participation of other elements such as: Th17 or IL-17, IL-23, IL-25, IL-27, Tregs, TLRs, NODs, MAs, DCs, bronchial epithelial cells, chemokines, neurokinins, ICAM-1, NO (iNO). Besides other elements that influence the inflammatory response amplification and the remodeling of the airway epithelium.
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PMID:[Pathogenesis, trigger and risk factors in asthma]. 2087 49

Liver granulomas and elevated serum IgM are commonly observed in patients with primary biliary cirrhosis (PBC) but their pathogenetic significance remains largely unknown. To address this issue we performed an extensive immunostaining and colocalization study of markers associated with dendritic cells and IgM in a large cohort of tissue samples from PBC and control livers as well as from non-hepatic granulomatous diseases. First, the classical dendritic cell CD11c marker is highly expressed and more sensitive than classical hematoxylin-eosin staining in detecting granulomas associated with PBC and other conditions. Second, PBC cases with CD11c-positive granulomas have significantly higher serum IgM levels and earlier disease stages. Third, granulomas from PBC and other diseases demonstrate markers of dendritic cell immaturity, i.e. CD11b, reduced MHC II, IL-23, CCR7 and CD83 expression, and elevated C1q expression. Lastly, B cells and IgM-positive plasma cells are largely represented around PBC granulomas along with macrophages. In conclusion, our comprehensive immunohistochemical study suggests that dendritic cells are key to the pathogenesis of granulomas, regardless of their origin. More specifically, PBC liver granulomas may result from the interaction between immature dendritic cells and IgM.
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PMID:The immunopathology of liver granulomas in primary biliary cirrhosis. 2272 62