The cytokine receptor family type 2 (CRF2) comprises receptors for important immunomediators like interferons and interleukin-10 (IL-10). We identified a novel member of this family which represents the first exclusively soluble receptor in this group and was therefore designated as CRF2-soluble 1 (CRF2-s1). The CRF2-s1 gene covers about 28 kb and is located on chromosome 6 in close proximity to the CRF2 members interferon (IFN)-gamma receptor 1 and IL-20 receptor 1. It comprises seven exons and generates two different mRNA splice variants, CRF2-s1-long and CRF2-s1-short. CRF2-s1-long and CRF2-s1-short encode proteins of 263 and 231 amino acids, respectively. A comparison of predicted protein structures led to the postulation that each receptor variants binds a different ligand. Quantitative analysis of human mRNA expression revealed a very restricted pattern for both splice forms. CRF2-s1 turned out to be the first member of this receptor family which was expressed neither in resting nor in stimulated leucocyte populations. CRF2-s1-long was only expressed in placenta, whereas CRF2-s1-short was additionally expressed in human mammary gland and, at a lower level, in skin, spleen, thymus and stomach. The preferential expression of CRF2-s1 in placenta suggests a role for this receptor in establishing and maintaining successful pregnancy.

We have identified the mouse and rat homologs of human interleukin-22 receptor alpha 2 (IL-22R alpha 2) and compared the localization, structure, and expression of the encoding murine and human genes. The mouse IL-22R alpha 2-encoding gene is located on chromosome 10A3 between, like in human, the genes for interferon-gamma R1 and IL-20R1. It spans a region of approximately 10 kb therefore being three times shorter than the human gene. Although the overall gene structure in both species is similar, the mouse gene lacks a counterpart to the third coding exon of the human gene known to be alternatively spliced. Like in human, mouse and rat IL-22R alpha 2 exist only as soluble receptors as deduced from the lack of transmembrane and intracellular domains encoding sequences. Quantitative expression analyses showed, analogically to the human system, a limited tissue distribution of mouse IL-22R alpha 2 mRNA. Differential modulation of IL-22R alpha 2 mRNA expression was observed upon systemic inflammation in mice in spleen, thymus, and lymph node.

Normal myeloid and MGI+D+ clones of myeloid leukemic cells can be induced for Fc and complement component 3 rosettes, lysozme, and mature macrophages and granulocytes by a protein with macrophage-and granulocyteinducing (MGI) activity, whereas MGI+D-clones can be induced by this protein for rosettes and Iysozme but not mature cells. Lipopolysaccharides (LPS) (14), and mature cells (6,8,9), whereas other clones (MGI+D-) can be induced for rosettes and lysozme but not for mature cells (10,14). The inducing activity (1-4) that we now call MGI has also been referred to as "colony-stimulating" factor (15) or activity (16). Some of the stages of differentiation can be induced in MGI+D+ clones by certain steroid hormones (10,17) and compounds such as cytosine arabinoside, actinomycin D, 5-iododeoxyuridine, and dimethyl sulfoxide (10,14,18).Bacterial lipopolysaccharides (LPS) are presumably surface-acting compounds that can induce various changes including stimulation of cell multiplication and antibody formation by B lymphocytes (19,20), production of pyrogens, and cytotoxicity (21-23). It has been shown that the active part of LPS in inducing these changes is lipid A (19-23). The present experiments were undertaken to determine whether LPS from different bacteria can induce differentiation of myeloid leukemic cells, whether the active part of the molecule is lipid A,The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertwsement" in accordance with 18 U. S C §1734 solely to indicate this fact. and whether induction of differentiation by this presumably surface-acting compound is direct or is indirect by inducing the production of MGI in the myeloid leukemic cells. MATERIALS AND METHODSCells and Cell Cultures. MGI+D+ clones 9, 11, 12, and 21 and MGI+D-clones 2,5, and 13 (9, 10) were obtained from a cell line of myeloid leukemia originating in an SL mouse (24). All the clones grew in suspension as myeloblasts or promyelocytes and produced leukemia after inoculation into isologous adult mice. Normal mature macrophages were collected from the peritoneal cavity of SL mice at 3 days after intraperitoneal injection of 1 sodium caseinate (Difco)

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