It is generally acknowledged that infancy and early childhood are high risk periods for infectious diseases, particularly those of viral origin (1, 2). Antivira immunity during primary infection appears diminished (3-5), and this appears to be accompanied by a general failure of neonatal anti-viral T-cell responses to mature into protective virus-specific immunological memory (6). This maturational deficiency is even more pronounced in premature infants, and additionally manifests in this group as sluggish anti-vaccine responses, associated with both low IgG antibody production and reduced numbers of virus-specific T-cells in PBL during the post vaccination period (6). Resistance to bacterial and fungal infections is also less effective (7), suggesting accompanying deficiencies in innate immune mechanisms. The seroepidemiological literature pertaining to atopic diseases, particularly prospective studies on cohorts of atopic and normal children, indicates that primary allergic sensitisation to environmental allergens most commonly occurs during this same period (reviewed in S), and this appears to result primarily from a malfunction in neonatal mucosal tolerance induction mechanisms (9, 10). Given the central role of adaptive immune processes in the aetiology of atopy, it is reasonable to speculate that the heightened susceptibility of infants to primary allergic sensitisation is also likely to stem from transient maturational defects in immune function, similar to those underlying decreased resistance to infection. Recent developments in a number of areas in basic cellular immunology reviewed below, are providing new insights into the precise nature of the maturational deficiencies in immune function in early postnatal life.

Postnatal maturation of immune competence during infancy and childhood.

A retroplacental serum factor responsible for the downregulation of the MHC class II antigen expression has been described [1]. We found that maternal serum had the same property. The HLA class II modulating activity is however diminished in the presence of maternal serum as compared to retroplacental serum suggesting that the IA like inhibiting factor is released at the fetomaternal interface. After a 3-day incubation period of unrelated lymphocytes and mononuclear cord blood cells in a maternal serum pool, it was shown that the HLADr, the HLADp, and more significantly, the HLADq molecules were modulated. This phenomenon was more pronounced among cord blood cells. When third party lymphocytes and mononuclear cord blood cells were stimulated by Candidine or unrelated mononuclear cells in the presence of retroplacental serum, only the cellular subpopulation belonging to the CD4+ subset showed an HLADq downregulation. The molecular constituents of the MHC class II antigen expression characterizing cells belonging to other subsets remained unchanged. When the same stimulation assay was performed in the presence of a control medium (nulliparous serum), we found no changes in the MHC class II molecular constituents. When unrelated mononuclear cells and mononuclear cord blood cells were PHA stimulated in the presence of maternal and nulliparous serum, the HLADq expression of the CD8+ subset showed a significant downregulation in the maternal serum mediated stimulation assay as compared to the control stimulation test. The molecular expression of the HLA class II antigen related to the other subpopulation (CD4+, CD3+) stimulated by a mitogenic lectin remained unchanged. It is suggested that these molecular MHC class II modulations are due to a factor included in the maternal IgG reaction. Retroplacental IgG contains the highest concentration of this factor.

Modulation of the HLA class II antigen at a molecular level by maternal serum among cord blood cells and unrelated lymphocytes.

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Modulation of the HLA class II antigen at a molecular level by maternal serum among cord blood cells and unrelated lymphocytes.