Abstract: Disclosed are methods, nucleic acids, and cells for expressing an exogenous gene in a mammalian cell, involving introducing into the cell a non-mammalian DNA virus (e.g., a baculovirus) having an altered coat protein, the genome of which virus carries an exogenous gene, and growing the cell under conditions such that the gene is expressed. Also disclosed are methods for treating gene deficiency disorders, neurological disorders, or cancers in a mammal by (1) providing to a cell a therapeutically effective amount of a non-mammalian DNA virus having an altered coat protein, the genome of which virus carries an exogenous, therapeutic gene and (2) growing the cell under conditions such that the exogenous gene is expressed in the mammal.

Abstract: Disclosed are methods, nucleic acids, and cells for expressing an exogenous gene in a mammalian cell, involving (i) introducing into the cell a complement-resistant non-mammalian DNA virus (e.g., a baculovirus), optionally having an altered coat protein, the genome of which virus carries an exogenous gene, and (ii) growing the cell under conditions such that the gene is expressed.

Abstract: CAIP polypeptide, nucleic acids, ands uses thereof. A method of evaluating a compound for the ability to bind a CAIP polypeptide; fragment or analog thereof is described.

Abstract: Methods of using inhibitors of the CD2/LFA-3 interaction in treating skin conditions characterized by increased T cell activation and abnormal antigen presentation in the dermis and epidermis in mammals, including humans. Such conditions include psoriasis, UV damage, e.g., photoaging, atopic dermatitis, cutaneous T cell lymphoma such as mycosis fungoides, allergic and irritant contact dermatitis, lichen planus, alopecia areata, pyoderma gangrenosum, vitiligo, ocular cicatricial pemphigoid, and urticaria.

Abstract: A IFN-.beta. mutein in which phe (F), tyr (Y), trp (W) or his (H) is substituted for val (V) at position 101, when numbered in accordance with wild type IFN-.beta., DNA sequences encoding these IFN-.beta. muteins, recombinant DNA molecules containing those DNA sequences operatively linked to expression control sequences and capable of inducing expression of an IFN-.beta. mutein, hosts transformed with those recombinant DNA molecules, pharmaceutical compositions containing IFN-.beta. muteins and methods for treating viral infections, cancer or tumors, undesired cell proliferation, or for immunomodulation.

Abstract: A method for the treatment of inflammatory bowel disease (IBD) is disclosed. The method comprises administration of an antibody, polypeptide or other molecule recognizing VLA-4, a surface molecule expressed on most types of white blood cells and involved in leukocyte adhesion to endothelium and other tissus in the gut.

Abstract: Polypeptides and proteins comprising the CD2-binding domain of LFA-3 are disclosed. DNA sequences that code on expression for those polypeptides and proteins, methods of producing and using those polypeptides and proteins, and therapeutic and diagnostic compositions are also disclosed. Deletion mutants unable to bind CD2 and methods for their use are also disclosed. In addition, fusion proteins which comprise the CD2-binding domain of LFA-3 and a portion of a protein other than LFA-3, DNA sequences encoding those fusion proteins, methods for producing those fusion proteins, and uses of those fusion proteins are disclosed.

Abstract: This invention relates to compositions and methods comprising "lymphotoxin-.beta. receptor blocking agents", which block lymphotoxin-.beta. receptor signalling. Lymphotoxin-.beta. receptor blocking agents are useful for treating lymphocyte-mediated immunological diseases, and more particularly, for inhibiting Th1 cell-mediated immune responses. This invention relates to soluble forms of the lymphotoxin-.beta. receptor extracellular domain that act as lymphotoxin-.beta. receptor blocking agents. This invention also relates to the use of antibodies directed against either the lymphotoxin-.beta. receptor or its ligand, surface lymphotoxin, that act as lymphotoxin-.beta. receptor blocking agents. A novel screening method for selecting soluble receptors, antibodies and other agents that block LT-.beta. receptor signalling is provided.

Abstract: Polypeptides and proteins comprising the CD2-binding domain of LFA-3 are disclosed. DNA sequences that code on expression for those polypeptides and proteins, methods of producing and using those polypeptides and proteins, and therapeutic and diagnostic compositions are also disclosed. Deletion mutants unable to bind CD2 and methods for their use are also disclosed. In addition, fusion proteins which comprise the CD2-binding domain of LFA-3 and a portion of a protein other than LFA-3, DNA sequences encoding those fusion proteins, methods for producing those fusion proteins, and uses of those fusion proteins are disclosed.

Abstract: A method for the prevention of insulin dependent (type I) diabetes. The method comprises administration of an antibody, polypeptide or other molecule recognizing VLA-4.

Abstract: A method for the treatment of asthma is disclosed. The method comprises administration of an antibody, polypeptide or other molecule recognizing VLA-4, a protein expressed on the surface of certain leukocytes such as eosinophils.

Abstract: Anti-CD4 antibody homologs, DNA sequences and recombinant DNA molecules encoding them, prophylactic, immunotherapeutic and diagnostic compositions comprising those antibody homologs, and methods for preventing or treating diseases in mammals, including humans, caused by infective agents whose primary targets are CD4.sup.+ lymphocytes. Such diseases include acquired immune deficiency syndrome ("AIDS"), AIDS related complex, and human immunodeficiency virus infection.

Abstract: The present invention relates to uses of mutant proto-oncogenes and oncoproteins expressed by the proto-oncogenes in inhibiting tumor growth and/or inhibiting the transformed phenotype. The preferred oncoprotein is a dominant, interfering mutant of a nuclear E2F transcription factor protein and is preferably a mutant E2F1 transcription factor protein. Methods of treating a target cell are described. Treatment is accomplished by administering to a target cell a dominant interfering mutant of a proto-oncogene in an effective amount. Treatment is also accomplished by administering to a target cell an oncoprotein in an effective amount. Compositions for such use are described as well.

Abstract: An isolated nucleic acid encoding a CD2 Associated Intracellular Protein (CAIP) and uses thereof.

Abstract: This invention relates to delivery of biologically active cargo molecules, such as polypeptides and nucleic acids, into the cytoplasm and nuclei of cells in vitro and in vivo. Intracellular delivery of cargo molecules according to this invention is accomplished by the use of novel transport polypeptides which comprise HIV tat protein or one or more portions thereof, and which are covalently attached to cargo molecules. The transport polypeptides in preferred embodiments of this invention are characterized by the presence of the tat basic region (amino acids 49-57), the absence of the tat cysteine-rich region (amino acids 22-36) and the absence of the tat exon 2-encoded carboxy-terminal domain (amino acids 73-86) of the naturally-occurring tat protein. By virtue of the absence of the cysteine-rich region, the preferred transport polypeptides of this invention solve the potential problems of spurious trans-activation and disulfide aggregation.

Abstract: This invention relates to lymphotoxin-.beta., a lymphocyte membrane type protein. This protein is found on the surface of a number of cells, including phorbol ester (PMA) stimulated T cell hybridoma II-23.D7 cells. This invention also relates to complexes formed between lymphotoxin-.beta. and other peptides such as lymphotoxin-.alpha. and to complexes comprising multiple subunits of lymphotoxin-.beta.. These proteins and complexes are useful in holding LT-.alpha. formed within the cell on the cell surface where the LT-.alpha./LT-.beta. complex may act as an inflammation regulating agent, a tumor growth inhibiting agent, a T cell inhibiting agent, a T cell activating agent, an autoimmune disease regulating agent, or an HIV inhibiting agent. Furthermore, the antitumor activity of the LT-.alpha./LT-.beta. complex may be delivered to tumor cells by tumor infiltrating lymphocytes (TILs) transfected with the gene for LT-.beta..

Abstract: Polypeptides and proteins comprising the CD2-binding domain of LFA-3 are disclosed. DNA sequences that code on expression for those polypeptides and proteins, methods of producing and using those polypeptides and proteins, and therapeutic and diagnostic compositions are also disclosed. Deletion mutants unable to bind CD2 and methods for their use are also disclosed. In addition, fusion proteins which comprise the CD2-binding domain of LFA-3 and a portion of a protein other than LFA-3, DNA sequences encoding those fusion proteins, methods for producing those fusion proteins, and uses of those fusion proteins are disclosed.

Abstract: This invention relates to novel biologically active molecules which bind to and inhibit thrombin. Specifically, these molecules are characterized by a thrombin anion-binding exosite association moiety (ABEAM); a linker portion of at least 18 .ANG. in length; and a thrombin catalytic site-directed moiety (CSDM). This invention also relates to compositions, combinations and methods which employ these molecules for therapeutic, prophylactic and diagnostic purposes.

Abstract: The present invention relates to therapeutic methods wherein an actin-binding protein, preferably gelsolin or DBP, is administered to a patient with actin-containing clots in order to remove actin from the clots. The invention also relates to diagnostic methods in which actin is removed from an actin-containing clot in vitro and quantitated.

Abstract: This invention relates to lymphotoxin-.beta., a lymphocyte membrane type protein. This protein is found on the surface of a number of cells, including phorbol ester (PNA) stimulated T cell hybridoma II-23.D7 cells. This invention also relates to complexes formed between lymphotoxin-.beta. and other peptides such as lymphotoxin-.alpha. and to complexes comprising multiple subunits of lymphotoxin-.beta.. These proteins and complexes are useful in holding LT-.alpha. formed within the cell on the cell surface where the LT-.alpha./LT-.beta. complex may act as an inflammation regulating agent, a tumor growth inhibiting agent, a T cell inhibiting agent, a T cell activating agent, an autoimmune disease regulating agent, or an HIV inhibiting agent. Furthermore, the antitumor activity of the LT-.alpha./LT-.beta. complex may be delivered to tumor cells by tumor infiltrating lymphocytes (TILs) transfected with the gene for LT-.beta..