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TY - JOUR AU - Burkly, Linda AU - Hession, Catherine AU - Ogata, Lynn AU - Reilly, Christina AU - Marconl, Lori Anne AU - Olson, Dian AU - Tizard, Richard AU - Gate, Richard AU - Lo, David PY - 1995 DA - 1995/02/01 TI - Expression of relB is required for the development of thymic medulla and dendritic cells JO - Nature SP - 531 EP - 536 VL - 373 IS - 6514 AB - DENDRITIC cells (DC) derived from bone marrow are critical in the function of the immune system, for they are the primary antigen-presenting cells in the activation of T-lymphocyte response. Their differentiation from precursor cells has not been defined at a molecular level, but recent studies have shown an association between expression of the relB subunit of the NF-κB complex1–5 and the presence of DC in specific regions of normal unstimulated lymphoid tissues4–6. Here we show that relB expression also correlates with differentiation of DC in autoimmune infiltrates in situ, and that a mutation disrupting the relB gene results in mice with impaired antigen-presenting cell function, and a syndrome of excess production of granulocytes and macrophages. Thymic UEA-1+ medullary epithelial cells from normal mice show striking similarities to DC and, interestingly, these cells are also absent in relB mutant mice. Taken together, these results suggest that relB is critical in the coordinated activation of genes necessary for the differentiation of two unrelated but phenotypically similar cells (DC and thymic UEA-1+ medullary epithelial cells) and is therefore a candidate for a gene determining lineage commitment in the immune system. SN - 1476-4687 UR - https://doi.org/10.1038/373531a0 DO - 10.1038/373531a0 ID - Burkly1995 ER -