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A pulmonary ILC3 niche promotes neonatal mucosal immunity to respiratory bacterial infection and is associated with postnatal lung development.

08:00 EDT 17th March 2020 | BioPortfolio

Summary of "A pulmonary ILC3 niche promotes neonatal mucosal immunity to respiratory bacterial infection and is associated with postnatal lung development."

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This article was published in the following journal.

Name: Mucosal immunology
ISSN: 1935-3456
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Medical and Biotech [MESH] Definitions

Nonsusceptibility to the pathogenic effects of foreign microorganisms or antigenic substances as a result of antibody secretions of the mucous membranes. Mucosal epithelia in the gastrointestinal, respiratory, and reproductive tracts produce a form of IgA (IMMUNOGLOBULIN A, SECRETORY) that serves to protect these ports of entry into the body.

Rare congenital metabolism disorders of the urea cycle. The disorders are due to mutations that result in complete (neonatal onset) or partial (childhood or adult onset) inactivity of an enzyme, involved in the urea cycle. Neonatal onset results in clinical features that include irritability, vomiting, lethargy, seizures, NEONATAL HYPOTONIA; RESPIRATORY ALKALOSIS; HYPERAMMONEMIA; coma, and death. Survivors of the neonatal onset and childhood/adult onset disorders share common risks for ENCEPHALOPATHIES, METABOLIC, INBORN; and RESPIRATORY ALKALOSIS due to HYPERAMMONEMIA.

A respiratory distress syndrome in newborn infants, usually premature infants with insufficient PULMONARY SURFACTANTS. The disease is characterized by the formation of a HYALINE-like membrane lining the terminal respiratory airspaces (PULMONARY ALVEOLI) and subsequent collapse of the lung (PULMONARY ATELECTASIS).

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A disorder of neuromuscular transmission that occurs in a minority of newborns born to women with myasthenia gravis. Clinical features are usually present at birth or develop in the first 3 days of life and consist of hypotonia and impaired respiratory, suck, and swallowing abilities. This condition is associated with the passive transfer of acetylcholine receptor antibodies through the placenta. In the majority of infants the myasthenic weakness resolves (i.e., transient neonatal myasthenia gravis) although this disorder may rarely continue beyond the neonatal period (i.e., persistent neonatal myasthenia gravis). (From Menkes, Textbook of Child Neurology, 5th ed, p823; Neurology 1997 Jan;48(1):50-4)

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