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We have identified the human gene, SCL. We discovered this gene because of its involvement in a chromosomal translocation associated with the occurrence of a stem cell leukemia manifesting myeloid and lymphoid differentiation capabilities. Here we report the sequence of a cDNA for the normal SCL transcript, as well as for an aberrant fusion transcript produced in the leukemic cells. Although different at their 3' untranslated regions, both cDNAs predict a protein with primary amino acid sequence homology to the previously described amphipathic helix-loop-helix DNA binding and dimerization motif of the Lyl-1, myc, MyoD, immunoglobulin enhancer binding, daughterless, and achaete-scute families of genes. For these cDNAs, at least two different 5' ends are predicted, both of which retain this putative DNA binding domain and predict proteins in the range of 20-30 kDa. SCL mRNA is observed in "early" hematopoietic tissues. Taken together, these studies lead to the speculation that SCL plays a role in differentiation and/or commitment events during hematopoiesis.

This study provides the first description of TF protein expression in human coronary artery lesions in vivo. Tissue factor was readily detected in de novo lesions in patients with unstable coronary syndromes, suggesting a role for TF in the pathogenesis of this disease process. Conversely, TF was rarely detected in patients with restenosis lesions even if the resulting clinical presentation was an unstable coronary syndrome. These results may have implications for the management of patients with unstable angina from de novo lesions and patients with ischemic symptoms from a restenosis lesion.

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Individuals infected by the human immunodeficiency virus type 1 (IV-i) demonstrate progressive de-

Cellular interactions between developing thymocytes and cells of the thymic microenvironment are necessary for maturation of thymocytes into mature T cells. While much is known about the molecules on developing T cells that mediate these interactions, little is known about the surface molecules of human thymic epithelial (TE) cells. In this study, using a panel of 276 MAb including 255 MAb from the 5th International Workshop on Human Leukocyte Differentiation Antigens (HLDA-V), we have determined the expression of CD1 through CDw130 and other surface molecules on resting and IFN-gamma-activated cultured human TE cells and on resting epidermal keratinocytes (EK). We demonstrate the surface expression of 50 of the 161 molecules assayed for on TE cells, including a number of adhesion molecules, cytokine receptors, Apo-1, and MHC-encoded molecules. While activation of TE cells with IFN-gamma for 48 hr induced a greater than fivefold increase in the expression of four surface molecules (CD38, CD54, MHC class I, and MHC class II), it also induced a greater than 50% increase in the expression of 14 other surface molecules (CD12, CD29, CD40, CD44, CD47, CD49b, CD49c, CD49e, CD55, CD66, CD87, CD104, TE4, and STE3) and a decrease in the expression of three molecules (CDw65, CDw109, and STE2). In comparing the phenotype of TE cells to 83 other cell lines studied in HLDA-V, we found that TE cells were strikingly more similar to EK than to any of the other cell types tested.

To study the role that epithelial cells of the thymic microenvironment play in promoting activation of immature CD7+, CD2+, CD4-, CD8-(double-negative) human thymocytes, we have isolated thymocyte subsets from normal postnatal thymus and have cocultured autologous double-negative thymocytes with pure populations of thymic epithelial (TE) cells. We report that TE cells directly activate double-negative thymocytes to proliferate and that TE cells enhance the ability of double-negative thymocytes to proliferate in response to stimulation with exogenous interleukin 2. Activated double-negative thymocytes that proliferated in vitro in the presence of TE cells and interleukin 2 remained doublenegative after 23 days in culture. Moreover, TE-cell culture supernatants in the absence of intact TE cells contain interleukin 1, interleukin 3, and granulocyte/macrophage-colonystimulating factor activity for human bone marrow cells and can activate double-negative thymocytes to proliferate. Antibodies against interleukin 1 and against granulocyte/macrophage-colony-stimulating factor inhibited TE-cell-induced thymocyte activation. These data indicate that one role of TE cells in vivo may be to activate double-negative thymocytes to proliferate.The thymus is known to be the primary site of T-cell maturation during fetal and neonatal development (1)(2)(3)(4)(5). However, specific cellular interactions and activation signals necessary for growth and differentiation of T-cell precursors within the human thymus are largely unknown (4-6). Studies of T-cell ontogeny in mice have suggested that the earliest intrathymic T cells have the surface phenotype dLytl + ("d" means that the immunofluorescence is faint, or "dull"), Lyt2-, L3T4-and that a subpopulation of dLytl +, Lyt2 -, L3T4-thymocytes are able to reconstitute the T-cell repertoire (7-13).Lobach and Haynes (14) showed that, during human fetal development, the earliest T-cell precursors are CD7+ prior to entry into the thymus, and these cells acquire the CD2, CD4, CD8, CD3, and CD1 molecules in the thymus between 82 and 14 weeks of fetal gestation. At 8½ weeks of fetal development, intrathymic T cells are CD7+, CD2+, CD4-, CD8-(double-negative) (14)(15)(16).To study the role that thymic epithelial (TE) cells might play in activating subsets of human double-negative thymocytes to proliferate and differentiate into mature T cells, we developed an in vitro coculture system of autologous TE cells and double-negative thymocytes (17). Here we show that TE cells up-regulate interleukin 2 (IL-2) receptor expression and IL-2 responsiveness of double-negative thymocytes and directly activate immature thymocytes to proliferate.Moreover, TE cells produce cytokines capable of providing activation signals to double-negative thymocytes in the absence of direct TE-cell-thymocyte contact.

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