SummaryNatural killer (NK) cells have been defined as CD3e -,CD16 + and/or CD56 § lymphocytes that mediate major histocompatibility complex (MHC)-unrestricted cytotoxicity against certain tumors and virus-infected cells. Unlike T lymphocytes, NK cells do not rearrange or productively express T cell antigen receptor genes. Moreover, NK cells from adults have been reported to not express CD3% & or e proteins on the cell surface or in the cytoplasm. Nonetheless, NK cells have been shown to share a number of antigenic and functional similarities to T cells that suggest the possibility of common origins. In this report, we demonstrate that functional NK cells exist in liver at early stages of human embryonic development. Freshly isolated fetal NK cells mediated MHC-unrestricted cytotoxicity against NK-sensitive targets and acquired the ability to lyse NKresistant tumors after overnight culture in interleukin 2. Unlike adult NK cells, freshly isolated fetal liver NK cells and clones derived from these cells, as well as a subset of cord blood NK cells, express substantial levels of CD36 and CD3e proteins in the cytoplasm. Expression of CD3e and CD3~ transcripts and cytoplasmic proteins in fetal NK clones was confirmed by polymerase chain reaction and Western blot analysis. These findings support the concept that NK and T cells may arise from a common progenitor that expresses components of the CD3 complex. Alternatively, it is possible that the cytoplasmic CD36,e § fetal NK cells represent a distinct subpopulation of NK cells that is predominant in the fetus, but replaced by the cytoplasmic CD3~,e-adult NK cell population after embryogenesis.

Dendritic cells (DCs) can induce and control host immune responses. DC subset-dependent functional specialties and their ability to display functional plasticity, which is mainly driven by signals via pattern-recognition receptors (PRRs), identify DCs as immune orchestrators. A PRR, Dectin-1 is expressed on myeloid DCs (mDCs) and is known to play an important role in TH17 responses. Here, we demonstrate that human plasmacytoid DCs (pDCs) express Dectin-1. Interestingly, Dectin-1-activated pDCs promote TH2 induction and activation, whereas Dectin-1-activated mDCs decrease both. This counter-regulation of TH2 by the two DC subsets is mainly due to their distinct abilities to control OX40L expression through different mechanisms. This study provides new insights for the regulation of host immune responses by DCs during microbial infections.