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

: Subtle increases in immaturity of immune function in early infancy have been implicated in the rising susceptibility to allergic disease, particularly relative impairment of type 1 interferon (IFN)-gamma responses in the neonatal period. Although genetic predisposition is a clear risk factor, the escalating rates of allergic disease in infancy suggest that environmental factors are also implicated. We previously showed that maternal smoking in pregnancy may impair neonatal IFN-gamma responses. Our more recent studies now indicate that this common avoidable toxic exposure is also associated with attenuation of innate immune function, with attenuated Toll-like receptor (TLR)-mediated microbial responses (including TLR-2, -3, -4, and -9 responses). Most notably, the effects were more marked if the mothers were also allergic. In this review, we discuss the significance of these observations in the context of the emerging hypothesis that variations in TLR function in early life may be implicated in allergic propensity. There is now growing evidence that many of the key pathways involved in subsequent T-cell programming and regulation (namely, antigen-presenting cells and regulatory T cells) rely heavily on microbe-driven TLR activation for maturation and function. Factors that influence the function and activity of these innate pathways in early life may contribute to the increasing predisposition for allergic disease. Although "cleaner" environments have been implicated, here we explore the possibility that other common environmental exposures (such as maternal smoking) could also play a role.
Allergy Asthma Clin Immunol 2007 Mar 15
PMID:Maternal smoking in pregnancy: do the effects on innate (toll-like receptor) function have implications for subsequent allergic disease? 2052 48

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.
 ...
PMID:[Pathogenesis, trigger and risk factors in asthma]. 2087 49

Acute otitis media (AOM) is a common disease in young children. Streptococcus pneumoniae (Spn) and Haemophilus influenzae (NTHi) are the two most common pathogens that cause AOM. Over the past 5 years, our group has been studying the immunologic profile of children that experience repeated AOM infections despite tympanocentesis drainage of middle ear fluid and individualized antibiotic treatment; we call these children stringently-defined otitis prone(sOP). Although protection against AOM is primarily mediated by ototpathogen-specific antibody, our recent studies suggest that suboptimal memory B and T cell responses and an immaturity in antigen-presenting cells may play a significant role in the propensity to recurrent AOM infections. This review focuses on the studies performed to define immunologic dysfunction in sOP children.
Curr Allergy Asthma Rep 2013 Oct
PMID:Cellular immune response in young children accounts for recurrent acute otitis media. 2402 64