CD3+/TCRαβ and CD3+/TCRγδ lymphocytes in full term neonates with early-onset pneumonia – influence of perinatal risk factors

Despite recent advances in neonatal intensive care and administration of broad-spectrum antimicrobial agents, early-onset pneumonia remains severe disease characterized by high mortality rate. Early-onset pneumonia (EOP) is caused by the infection of amniotic fluid via maternal perineum or genital tract, with clinical or subclinical chorioamnionitis. The incidence of EOP over a 41-month period in Oxford was 1,78 per 1000 live births [1]. EOP has been diagnosed at autopsy in 15-38% of stillborn and 2032% of live born babies who died [2]. Some authors emphasize, that the increase of mortality rate due to severe EOP is caused by weak and inappropriate immunity. Lymphoid tissue, apart from thymus is poorly developed in neonate. However, absolute number of T-cells in full-term neonates is comparable to values in older children. Although the ability of these cells to respond to various microbiological antigens is reduced, the agents can stimulate and activate proliferation and maturation of T-cells [3-5]. There is a lot of receptors on the surface of T-cell, but among them T-cell receptor (TCR) is considered to be the most characteristic. Discovery of TCR and explanation of its role in antigen recognition was made by Zinkernagel and CD3+/TCRαβ and CD3+/TCRγδ lymphocytes in full term neonates with early-onset pneumonia – influence of perinatal risk factors