Abstract: Human chemokine polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed.

Abstract: Human chemokine Beta-10 polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed.

Abstract: Human chemokine polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed.

Abstract: Human Chemokine Beta-10 polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed.

Abstract: Human chemokine Beta-10 polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed.

Abstract: Human HR-1 RECEPTOR polypeptides and DNA (RNA) encoding such HR-1 RECEPTOR genes and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such HR-1 RECEPTORS for the treatment of decreased level of resistance to infection, asthma, various allergic and hematopoietic disorders or a susceptibility to the aforementioned abnormalities. Antagonists against such HR-1 RECEPTOR and their use as a therapeutic to treat decreased level of resistance to infection, asthma, various allergic and hematopoietic disorders or a susceptibility to the aforementioned abnormalities are also disclosed. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Also disclosed are diagnostic assays for detecting mutations in the polynucleotides encoding the HR-1 RECEPTOR and for detecting altered levels of the polypeptide in a host.

Abstract: Human chemokine Beta-10 polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed.

Abstract: Disclosed are methods for discovering agonists and antagonists of the interaction between a secreted human protein, chemokine CK.beta.-9, and its cellular receptor, human CCR7, which may have utility in the treatment of several human diseases, including, but not limited to: allergic disorders, autoimmune diseases, ischemia/reperfusion injury, development of atherosclerotic plaques, cancer (including mobilization of hematopoietic stem cells for use in chemotherapy or mycloprotection during chemotherapy), chronic inflammatory disorders, chronic rejection of transplanted organs or tissue grafts, chronic myelogenous leukemia, and infection by HIV and other pathogens.

Abstract: Methods for the isolation of mutant rhizobial strains with improved competition of nodulation (Comp.sup.+) is presented. Mutants are selected for constitutive expression of inducible nod genes (in the absence of inducer) and screened for hyperinduction of nod genes in the presence of inducer. Mutants which are defective in nodulation or in symbiotic nitrogen fixation are eliminated from further testing. Selections for constitutive nod expression and for hyperinduction of nod genes are facilitated by the use of plasmid carrying a selectable marker fused to an inducible nod gene and a plasmid carrying a reporter gene fused downstream of an inducible nod gene. The methods exemplified are particularly useful for the isolation and identification of Comp.sup.+ mutants of Bradyrhizobium japonicum.

Abstract: The chemical compounds that induce expression of nodulation genes of Bradyrhizobium japonicum strains have been identified. The isoflavones daidzein and genistein were identified as soybean exudate components that induce nod-genes. Other isoflavones, including 7-hydroxyisoflavone, 5,7-dihydroxyisoflavone, biochanin A, formononetin and prunetin, were also found to act as inducers. In addition, several flavonoid compounds including 4',7-dihydroxyflavone, apigenin, kaempferol and coumestrol, were also found to act as inducers. Nodulation inducing compositions and a method for selectively activating the expression of a gene under the control of a soybean exudate inducible promoter in B. japonicum in response to these inducer molecules are described. In addition, soybean inoculating compositions containing the nod-gene inducers and inoculating methods employing these compositions are described.

Abstract: The isolation and characterization of nodD-related genes in soybean nodulating Rhizobium japonicum is described. In R. japonicum USDA 191 two such genes have been identified, which although related in structure, have different functional properties. These nodD genes are functionally distinct from each other and from those nodD genes of other strains of Rhizobium that have been isolated and characterized to date. In particular, nodD-r1 has been found to affect nodulation on soybean and to be associated with exopolysaccharide production. In contrast, nodD-r2 affects nodulation on the tropical legume siratro. The coding sequences of both nodD genes are provided. The promoter regions of the nodD genes have also been isolated. The genes described herein, including both structural genes and their promoter regions, can be used in combination with other genetic constructs to enhance the efficiency and competitiveness of nodulation.

Abstract: Nodulation regulatory genes (nodD genes) of Bradyrhizobium japonicum strains have been isolated and sequenced. Recombinant DNA molecules and vectors containing these regulatory genes are described. These genes, molecules and vectors are useful in the genetic engineering of Rhizobium and Bradyrhizobium strains. A method for selective expression of structural genes in response to the application of chemical factors which induce B. japonicum nod genes which employs these genes is described.

Abstract: A symbiosis plasmid from a fast-growing Rhizobium japonicum donor strain can be transferred to Rhizobium recipient strains, the recipient strains being previously incapable of forming an effective symbiotic relationship with plants of certain Glycine (e.g. soybean) varieties. The recipient strains harboring the symbiosis plasmid will form effective symbioses with soybean plants of said certain varieties, the transferred symbiosis plasmid conferring the host range or specificity of the donor strain on the recipient strains. Methods, strains, and plasmids useful for practice of this invention are also provided.

Abstract: The promoter of the nifH gene of the fast-growing Rhizobium japonicum strain USDA 191, has been cloned. Over 4.2 kilobase pairs (kbp) of DNA were sequences (FIG. 1). Sequences encoding nifH and the 5'-end of nifD were identified, as were sequences involved in promoting operon transcription and a nifH ribosome binding site. Use of the nifH promoter to drive transcription in Rhizobium of heterologous structural genes is taught. Useful sequences and plasmids are also disclosed.