Lymphocyte development begins early in the first trimester of gestation, and the fetus is capable of normal cytotoxic responses and some degree of T-B cooperation early in the second trimester. Neonates, however, are not fully immunocompetent at birth. They produce a restricted library of immunoglobulin isotypes and experience a ‘physiological hypogamma-globulinaemia’ for weeks or months. Premature infants are more profoundly hypogammaglobulinaemic for a longer time, and are less able to mount an appropriate response to bacterial or viral challenge, than term infants. Phenotypic analysis of lymphocyte populations from umbilical cord blood shows that lymphoid ontogeny is reflected in changing lymphoid subpopulations in peripheral blood of neonates throughout the third trimester of gestation. Immaturities exist in both B and T cell subsets in cord blood. These irregularities are most marked in early third trimester. Moreover, certain types of severe antenatal stress may alter the normal temporal sequence of acquisition of T and B lymphocyte surface antigens. The presence of T6+ cells in some cords suggests the possibility that profound stress, which causes the thymus to shrink, may also cause thymocytes to be released into circulation before the normal sequence of maturation is complete. These lymphocytes may be analogous to the ‘leftward shifted’ neutrophil band forms which are released into circulation in response to bacterial infection. Finally, newborns in general, and severely stressed or very premature newborns in particular, are at increased risk from infection not only because their immune systems are inexperienced, but primarily because their circulating T and B lymphocytes are at a stage of differentiation which may not permit them to function effectively in response to antigenic challenge.
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号