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This review focuses on the biology of thrombopoietin (Tpo) during human development. It summarizes the current understanding on molecular biological aspects of Tpo, cellular effects of Tpo on fetal and neonatal megakaryopoiesis, regulation of Tpo production, and circulating Tpo concentrations in human fetuses and neonates. Some important aspects on the developmental biology of Tpo are highlighted. They include the finding of high Tpo gene expression in the bone marrow during the onset of medullary hematopoiesis, higher circulating Tpo concentrations in fetuses and neonates than in children or adults, and a higher sensitivity of neonatal megakaryocyte progenitor cells to Tpo. However, other aspects of the developmental biology of Tpo are incompletely understood. Conclusion: More carefully designed studies are needed to provide the necessary background for an optimal treatment of fetal and neonatal thrombocytopenia.

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Aim: To determine whether an imbalance of dendritic cell subsets might contribute to diminished adaptive host responses observed in newborn infants. It was hypothesized that the proportion of lymphoid dendritic cells would be greater than that of myeloid dendritic cells in cord blood. Methods: To investigate this, dendritic cell subsets were evaluated in whole cord blood by flow cytometry. Circulating dendritic cells were also isolated from cord blood based on CD1c and BDCA‐2 expression. Myeloid dendritic cells were also obtained by culturing cord and adult blood monocytes. Surface phenotypes of these cells were determined by flow cytometry using monoclonal antibodies directed against lineage, major histocompatibility, adhesion, co‐stimulation and cytokine receptor molecules. Antigen‐presenting functions of dendritic cell subsets were determined by mixed leukocyte reactions. Results: Circulating myeloid dendritic cells were higher in cord blood than previously reported in adult blood, whereas lymphoid dendritic cell numbers were similar between cord and adult blood. Expression of CD11c, CD45RA and CD45RO did not accurately differentiate between dendritic cell subsets circulating in cord blood. Fresh and culture‐derived cord blood myeloid dendritic cells stimulated adult allogeneic leukocyte proliferation, while lymphoid dendritic cells were less effective inducers of an adult allogeneic leukocyte response. Culture‐derived dendritic cells induced modest autologous cord blood leukocyte proliferation, but freshly isolated myeloid and lymphoid dendritic cells did not stimulated autologous leukocytes. Conclusion: Contrary to the hypothesis, an imbalance in the ratio of circulating myeloid to lymphoid dendritic cell subsets does not exist and, therefore, does not contribute to diminished adaptive immune responses in newborn infants.