Neonates, particularly those born prematurely, are among the most vulnerable age group for morbidity and mortality due to infections. Immaturity of the innate immune system and a high need for invasive medical procedures in the context of a preterm birth make these infants highly susceptible to common neonatal pathogens. Preterm infants who survive may also suffer permanent disabilities due to organ damage resulting from either the infection itself or from the inflammatory response generated under an oxidative stress. Infections in preterm infants continue to pose important healthcare challenges. Yet, developmental maturation events in the innate immune system that underlie their excessively high vulnerability to infection remain largely understudied. In this review article, we identify pertinent knowledge gaps that must be filled in order to orient future translational research.
Fel d 4 is a lipocalin allergen produced by the cat, which binds IgE at relatively high frequency in cat-sensitive individuals. The allergen provides not only a means for investigating differences in the immune response to lipocalin allergens from that found for other mammalian species but also an important reagent for the diagnosis of cat allergy.
It has been shown previously that the in vitro response of mouse spleen cells to two types of sheep erythrocytes (high-H SRBC; low- L SRBC)2 is under multi-gene control (1). We have concluded that there are common or shared antigen(s) (C) found on both types of SRBC and extra antigen(s) (E) unique to H SRBC. The responses of spleen cell suspensions from various strains of mice to H SRBC have been divided into three categories: non-discriminator (ND), low-discriminator (LD), and high-discriminator (HD) based on the ratios of the number of plaque-forming cells (PFC) seen with H and L SRBC when the response is assayed after 4 days of culture (1). Only LD and HD mice are able to respond to the extra antigens on H SRBC. The in vitro response of discriminator mice to the C antigens is normal in LD and low in HD mice. This concept is illustrated in Table I.
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