Abstract: Disclosed herein are methods of treating disease with a combination of a RXR agonist and a thyroid hormone.

Abstract: A method of treating a disease, such as cancer, by administering to a subject in need of such treatment an effective amount of allogeneic T cells with a MHC unrestricted chimeric receptor short time after partial lymphodepletion. The method also comprises administering one or more agents that delay egression of the allogeneic T cells from lymph nodes of said subject during adoptive transfer of said allogeneic T cells to the subject by trapping the T cells in the lymph nodes.

Abstract: Disclosed herein are materials and methods for modulating an immunologically adverse response to an exogenous or endogenous immunogen, including a cell, tissue, or organ associated immunogen. An implantable material comprising cells, such as but not limited to endothelial cells, anchored or embedded in a biocompatible matrix can modulate an adverse immune or inflammatory reaction to exogenous or endogenous immunogens, including response to non-syngeneic or syngeneic cells, tissues or organs, exogenous immunogens or stimuli, as well as ameliorate an autoimmune condition. The implantable material can be provided prior to, coincident with, or subsequent to occurrence of the immune response or inflammatory reaction. The implantable material can induce immunological acceptance in a transplant patient, reduce graft rejection and reduce donor antigen immunogenicity.

Abstract: The invention relates to compositions and methods for treating a host infected with a pathogen. The composition comprising a population of polyclonal bispecific binding molecules that can target and eliminate a host cell infected with the pathogen. Methods for activating and arming cytotoxic immune cells with the composition for use in treating a patient infected with a pathogen are also provided.

Abstract: A method for stimulating the immune system in immunocompromised patients in order to treat opportunistic infection. The method involves the infusion of intentionally mismatched allogeneic cells. In order to prevent graft vs. host disease complications, the allogeneic cells can be irradiated prior to infusion.

Abstract: Materials and methods are provided to improve survival of lymph nodes and integration of lymph nodes into a lymphatic network, following lymph node transplantation. The treatment or prevention of lymphedema is also addressed. A method of lymph node transfer includes transferring or transplanting a lymph node or lymph node fragment in a mammalian subject; and administering a composition comprising an agent selected from the group consisting of Vascular Endothelial Growth Factor C (VEGF-C) polynucleotides, VEGF-C polypeptides, Vascular Endothelial Growth Factor D (VEGF-D) polynucleotides, and VEGF-D polypeptides to a perinodal site within 20 cm of the lymph node or lymph node fragment. In certain embodiments, the agent is present in the composition in an amount effective to promote survival of the lymph node and integration of the lymph node into a lymphatic network in the mammalian subject, at the site of transfer or transplantation.

Abstract: A method of manipulating allogeneic cells for use in allogeneic cell therapy protocols is described. The method provides a composition of highly activated allogeneic T-cells which are infused into immunocompetent cancer patients to elicit a novel anti-tumor immune mechanism called the “Mirror Effect”. In contrast to current allogeneic cell therapy protocols where T-cells in the graft mediate the beneficial graft vs. tumor (GVT) and detrimental graft vs. host (GVH) effects, the allogeneic cells of the present invention stimulate host T-cells to mediate the “mirror” of these effects. The mirror of the GVT effect is the host vs. tumor (HVT) effect. The “mirror” of the GVH effect is the host vs. graft (HVG) effect. The effectiveness and widespread application of the anti-tumor GVT effect is limited by the severe toxicity of the GVH effect. In the present invention, the anti-tumor HVT effect occurs in conjunction with a non-toxic HVG rejection effect.

Abstract: Materials and methods are provided to improve survival of lymph nodes and integration of lymph nodes into a lymphatic network, following lymph node transplantation. The treatment or prevention of lymphedema is also addressed. A method of lymph node transfer includes transferring or transplanting a lymph node or lymph node fragment in a mammalian subject; and administering a composition comprising an agent selected from the group consisting of Vascular Endothelial Growth Factor C (VEGF-C) polynucleotides, VEGF-C polypeptides, Vascular Endothelial Growth Factor D (VEGF-D) polynucleotides, and VEGF-D polypeptides to a perinodal site within 20 cm of the lymph node or lymph node fragment. In certain embodiments, the agent is present in the composition in an amount effective to promote survival of the lymph node and integration of the lymph node into a lymphatic network in the mammalian subject, at the site of transfer or transplantation.

Abstract: Gene-modified, inflammation-specific monocytes that comprise a 1-alpha-hydroxylase gene, where the 1-alpha-hydroxylase gene is expressed to produce functional 1-alpha-hydroxylase enzyme when the monocytes transdifferentiate into gene-modified, inflammation-specific macrophages. Gene-modified, inflammation-specific macrophages that comprise a 1-alpha-hydroxylase gene. A method for treating one or more than one inflammation-related condition or disease, the method comprising administering gene-modified, inflammation-specific monocytes that comprise a 1-alpha-hydroxylase gene, where the 1-alpha-hydroxylase gene is expressed to produce functional 1-alpha-hydroxylase enzyme when the monocytes transdifferentiate into gene-modified, inflammation-specific macrophages.

Abstract: A method of manipulating allogeneic cells for use in allogeneic cell therapy protocols is described. The method provides a composition of highly activated allogeneic T-cells which are infused into immunocompetent cancer patients to elicit a novel anti-tumor immune mechanism called the “Mirror Effect”. In contrast to current allogeneic cell therapy protocols where T-cells in the graft mediate the beneficial graft vs. tumor (GVT) and detrimental graft vs. host (GVH) effects, the allogeneic cells of the present invention stimulate host T-cells to mediate the “mirror” of these effects. The mirror of the GVT effect is the host vs. tumor (HVT) effect. The “mirror” of the GVH effect is the host vs. graft (HVG) effect. The effectiveness and widespread application of the anti-tumor GVT effect is limited by the severe toxicity of the GVH effect. In the present invention, the anti-tumor HVT effect occurs in conjunction with a non-toxic HVG rejection effect.

Abstract: A method of manipulating allogeneic cells for use in allogeneic cell therapy protocols is described. The method provides a composition of highly activated allogeneic T-cells which are infused into immunocompetent cancer patients to elicit a novel anti-tumor immune mechanism called the “Mirror Effect”. In contrast to current allogeneic cell therapy protocols where T-cells in the graft mediate the beneficial graft vs. tumor (GVT) and detrimental graft vs. host (GVH) effects, the allogeneic cells of the present invention stimulate host T-cells to mediate the “mirror” of these effects. The mirror of the GVT effect is the host vs. tumor (HVT) effect. The “mirror” of the GVH effect is the host vs. graft (HVG) effect. The effectiveness and widespread application of the anti-tumor GVT effect is limited by the severe toxicity of the GVH effect. In the present invention, the anti-tumor HVT effect occurs in conjunction with a non-toxic HVG rejection effect.

Abstract: The present invention discloses an immunotherapeutic method for treating patients suffering from malignant melanoma, by administering expanded tumour-reactive CD4+ helper and/or CD8+ T-lymphocytes obtainable from one or more sentinel or metinel lymph nodes draining a malignant melanoma or a metastasis arising from malignant melanoma. The present invention provides a new effective method for treating malignant melanoma and metastatic malignant melanoma, without adverse side effects associated with the known treatments.

Abstract: The present invention discloses an immunotherapeutic method for treating a patient suffering from a disseminated cancer by administering expanded tumour-reactive CD4+ helper and/or CD8+ T-lymphocytes obtainable from one or more metastasis-draining lymph nodes (metinel nodes) draining a metastasis. The method comprises identification of one or more metinel lymph nodes in a patient, resection of the one or more nodes and, optionally all or part of the metastases, isolation of metastasis-reactive T-lymphocytes from said lymph nodes, in vitro expansion of said metastasis-reactive T-lymphocytes, and administration of the thus obtained T-lymphocytes to the patient, wherein the T-lymphocytes are CD4+ helper and/or CD8+ T-lymphocytes.

Abstract: The present invention discloses an improved method for expansion and activation of tumor-reactive lymphocytes, in particular CD4+ helper and/or CD8+ T-lymphocytes, which may be used for treating and/or preventing cancer. The method provides high numbers of tumor-reactive T-lymphocytes within a short time span and the possibility of directing development of tumor-reactive CD4+ helper and/or CD8+ T-lymphocytes towards specific subpopulations. The method comprises a first phase of stimulating tumor-reactive CD4+ T helper and/or CD8+ T-lymphocytes with tumor-derived antigen together with at least one substance having agonistic activity towards the IL-2 receptor to promote survival of tumor-reactive CD4+ T helper and/or CD8+ T-lymphocytes; and a second phase of activating and promoting growth of tumor-reactive CD4+ T helper and/or CD8+ T-lymphocytes, wherein the second phase is initiated when the CD25 cell surface marker (or IL-2R marker) is down-regulated on CD4+ T helper and/or CD8+ T-lymphocytes.

Abstract: The present invention discloses an immunotherapeutic method for treating a patient suffering from urinary bladder cancer by administering expanded tumour-reactive CD4+ helper and/or CD8+ T-lymphocytes obtainable from one or more sentinel or metinel lymph nodes draining a tumour in the bladder or a metastasis arising from a tumour in the bladder. The method provides a new effective method for treating urinary bladder cancer and metastatic bladder cancer, without adverse side effects associated with the known treatments.

Abstract: Methods for treating a patient suffering from a neoplastic disease are disclosed and described. A number of diseases can be treated under the present methods, including without limitation gall bladder cancer, hepato cellular cancer, ovarian cancer, small intestine cancer, lung cancer, mesothelioma, breast cancer, kidney cancer, pancreas cancer, prostate cancer, carcinoid cancer, leiomyosarcoma, or metastasis thereof. A general method for providing such treatment may include: 1) identifying in a patient one or more sentinel and/or metinel lymph nodes draining the neoplasm; 2) resecting the one or more nodes and, optionally all or part of the tumour or metastasis; 3) isolating tumour-reactive T-lymphocytes from said lymph nodes; 4) in vitro expanding said tumour-reactive T-lymphocytes; and 5) administering the thus obtained tumour-reactive T-lymphocytes to the patient.

Abstract: A method of manipulating allogeneic cells for use in allogeneic cell therapy protocols is described. The method provides a composition of highly activated allogeneic T-cells which are infused into immunocompetent cancer patients to elicit a novel anti-tumor immune mechanism called the “Mirror Effect”. In contrast to current allogeneic cell therapy protocols where T-cells in the graft mediate the beneficial graft vs. tumor (GVT) and detrimental graft vs. host (GVH) effects, the allogeneic cells of the present invention stimulate host T-cells to mediate the “mirror” of these effects. The mirror of the GVT effect is the host vs. tumor (HVT) effect. The “mirror” of the GVH effect is the host vs. graft (HVG) effect. The effectiveness and widespread application of the anti-tumor GVT effect is limited by the severe toxicity of the GVH effect. In the present invention, the anti-tumor HVT effect occurs in conjunction with a non-toxic HVG rejection effect.

Abstract: Recent studies have demonstrated that lymphocyte-derived microparticles (LMPs) impair endothelial cell function. The present invention concerns the use of LMPs in the regulation of angiogenesis or diseases such as cancer or retinopathy of prematurity (ROP). Having long been considered as cellular debris, microparticles constitute reliable markers of vascular damage. Released into biological fluids, microparticles are involved in the modulation of key functions including immunity, inflammation, vascular remodeling and angiogenesis. The present data demonstrates that LMPs have considerable impact on angiogenesis in vitro and in vivo. In view of this, LMPs may be important contributors to the pathogenesis of diseases that are accompanied by impaired angiogenesis and could thus influence vascular function (microvascular angiogenesis and vasopermeability of ischemic tissue, alerting the body for special attention and the need for emergency repair procedures.

Abstract: The present invention provides devices and methods for concentrating a fluid and for treating a patient with the concentrated fluid. The concentrator apparatus includes a main housing (12) defining a separation chamber (14), a filter housing (48) containing a filter (46) comprising a filter element, a piping (44) for moving concentrated fluid from the separation chamber to the filter, and ports (32) for pressurizing the concentrated fluid past the filter element of the filter. The present invention also provides a variety of uses of concentrated body fluids, including autologous concentrated body fluid. The concentrated fluids can be used for example in surgical applications, including graft applications such as allograft, xenograft and autograft applications.

Abstract: Methods of forming proteinaceous products such as cell culture supplement capable of supporting the growth and culturing of cells, tissue, and organs, are generally disclosed. One method generally provides for the collection of the internal tissue of an animal, such as a bovine, and the processing of the internal tissue to degrade and/or lyse the tissue components. A cell culture supplement or other proteinaceous product can be prepared from the processed tissue. A proteinaceous product can include, for example, a complete protein profile of the tissue or only certain biological factors extracted from the tissue. Collected internal tissue can be lymphatic tissue such as the supramammary glands of a dairy or beef cow or the thymus gland of a veal calf.

Abstract: Methods for inducing antigen-specific T cell tolerance are disclosed. The methods involve contacting a T cell with: 1) a cell which presents antigen to the T cell, wherein a ligand on the cell interacts with a receptor on the surface of the T cell which mediates contact-dependent helper effector function; and 2) an antagonist of the receptor on the surface of the T cell which inhibits interaction of the ligand on the antigen presenting cell with the receptor on the T cell. In a preferred embodiment, the cell which presents antigen to the T cell is a B cell and the receptor on the surface of the T cell which mediates contact-dependent helper effector function is gp39. Preferably, the antagonist is an anti-gp39 antibody or a soluble gp39 ligand (e.g., soluble CD40). The methods of the invention can be used to induce T cell tolerance to a soluble antigen or to an allogeneic cell.

Abstract: Methods for generating highly enriched Th1/Tc1 and Th2/Tc2 functions are described. In particular, the generation of these functions are attained by the addition of an immune suppression drug, rapamycin or a rapamycin derivative compound. In addition to enhanced purity of T cell function, the T cells generated in rapamycin also express molecules that improve immune T cell function such as CD28 and CD62L. Such rapamycin generated functional T cell subsets may have application in the prevention or treatment of GVHD after allogeneic hematopoietic stem cell transplantation, the treatment of autoimmunity, or the therapy of infection or cancer.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: Conditioned media compositions having valuable biological activity are obtained from cultures of immune cells from elasmobranch fishes. A method is provided for producing the conditioned media compositions. Conditioned media obtained using epigonal cells from bonnethead sharks (Sphyrna tiburo) and lemon sharks (Negaprion brevirostris) demonstrate strong anti-tumor activities. The conditioned media compositions can be used for treating tumor proliferation.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: We teach a strategy to obtain large quantities of desired APCs, activated B cells, which are superior in their capacity to present tumor protein antigen in a multiadministration protocol. Human B cells can be obtained from peripheral blood in large numbers. These cells can be activated in vitro by coculture with CD40L (CD40-B cells) and an immunosuppressive agent such as cyclosporin A. They can expanded up to 1×103 to 1×104 fold in 2 weeks or 1×105 to 1×106 fold in 2 months. We demonstrate these cells are most efficient APCs comparable to DCs in stimulating allogeneic CD4+ CD45RA+, CD4+ CD45RO+, and CD8+ T cells. In contrast to DCs, CD40-B cells are fully functional even in the presence of immunosuppressive cytokines such as IL-10 and TGF?.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: The invention relates to a humanized anti-B7-2 antibody that comprises a variable region of nonhuman origin and at least a portion of an immunoglobulin of human origin. The invention also pertains to methods of treatment for various autoimmune diseases, transplant rejection, inflammatory disorders and infectious diseases by administering humanized anti-B7-2 and/or anti-B7-1 antibodies.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: Methods and compositions are described which allow for the sublingual absorption of peptides by oral administration. A liquid and a tablet format for the sublingual approach are demonstrated. The peptides are stable at room temperature and in the compositions herein described.

Abstract: The invention provides a method of determining whether a compound alleviates vasoconstriction-independent nerve pain mediated by endothelin-1 (ET-1). The method involves (i) determining whether the compound has the ability to inhibit a vasoconstriction-independent ET-1 action, and, if the compound has the inhibitory ability, then ii) determining whether the compound reduces vasoconstriction-independent nerve pain by testing the compound in human patients suffering from pain mediated by the vasoconstriction-independent ET-1 action. The invention also includes a method of determining whether a compound alleviates pain caused by nerve injury in human patients. The method involves (i) determining whether the compound has the ability to inhibit an inflammatory leukocyte response, and, if the compound has the inhibitory ability, then (ii) testing the compound in human patients suffering from pain caused by nerve injury to determine whether the compound alleviates the pain.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: Antigen-expressing, activated dendritic cells are disclosed. Such dendritic cells are used to present tumor, viral or bacterial antigens to T cells, and can be useful in vaccination protocols. Other cytokines can be used in separate, sequential or simultaneous combination with the activated, antigen-pulsed dendritic cells. Also disclosed are methods for stimulating an immune response using the antigen-expressing, activated dendritic cells.

Abstract: Methods for inducing antigen-specific T cell tolerance are disclosed. The methods involve contacting a T cell with: 1) a cell which presents antigen to the T cell, wherein a ligand on the cell interacts with a receptor on the surface of the T cell which mediates contact-dependent helper effector function; and 2) an antagonist of the receptor on the surface of the T cell which inhibits interaction of the ligand on the antigen presenting cell with the receptor on the T cell. In a preferred embodiment, the cell which presents antigen to the T cell is a B cell and the receptor on the surface of the T cell which mediates contact-dependent helper effector function is gp39. Preferably, the antagonist is an anti-gp39 antibody or a soluble gp39 ligand (e.g., soluble CD40). The methods of the invention can be used to induce T cell tolerance to a soluble antigen or to an allogeneic cell.

Abstract: The present invention provides a method of inducing systemic tolerance to an antigen in an individual in need of such treatment, comprising the step of: administering antigen presenting cells to said individual, wherein said cells express Fas ligand and said antigen.

Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.

Abstract: The invention is based on the discovery that substances which release ZAG proteins from lymphocytes also cause accelerated weight loss in humans. By administering an amount of the substance which is effective to cause the weight loss but is beneath an amount which causes side effects, a very desirable “dieter's aid” is provided. A dilute mixture of alfa interferon and gamma interferon in an aqueous medium is highly suitable for this purpose. It is administered at a much lower dosage than is generally employed for antibiotic purposes, thereby avoiding generally universal side effects. For periods of time extending at least for a few days, the weight loss composition of the invention causes weight loss at a greater weight than would be expected from fasting, at least for seriously overweight individuals.

Abstract: The present invention comprises homeopathic preparations of purified growth hormone, as well as methods and systems for delivery of such preparations and treatment of disorders and conditions by administering such preparations.

Abstract: The present invention provides vaccines and a means of vaccinating a vertebrate so as to prevent or control specific T cell mediated pathologies, including autoimmune diseases and the unregulated replication of T cells. The vaccine is composed of a T cell receptor (TCR) or a fragment thereof corresponding to a TCR present on the surface of T cells mediating the pathology. The vaccine fragment can be a peptide corresponding to sequences of TCRs characteristic of the T cells mediating said pathology. Such a peptide can bind to conventional antigens completed to MHC antigen presenting cells or to superantigens. Means of determining appropriate amino acid sequences for such vaccines are also provided. The vaccine is administered to the vertebrate in a manner that induces an immune response directed against the TCR of T cells mediating the pathology. This immune response down regulates or deletes the pathogenic T cells, thus ablating the disease pathogenesis.

Abstract: The present invention provides vaccines and a means of vaccinating a mammal so as to prevent or control specific T cell mediated pathologies or to treat the unregulated replication of T cells. The vaccine is composed of a T cell receptor (TCR) or a fragment thereof corresponding to a TCR present on the surface of T cells mediating the pathology. The vaccine fragment can be a peptide corresponding to sequences of TCRs characteristic of the T cells mediating said pathology. Means of determining appropriate amino acid sequences for such vaccines are also provided. The vaccine is administered to the mammal in a manner that induces an immune response directed against the TCR of T cells mediating the pathology. This immune response down regulates or deletes the pathogenic T cells, thus ablating the disease pathogenesis. The invention additionally provides a specific .beta.-chain variable region of the T cell receptor, designated V.beta.17, which is central to the pathogenesis of rheumatoid arthritis (RA).

Abstract: A method of treating a human cancer patient having a solid tumor comprising malignant cells is disclosed, wherein the patient having undergone a cancer therapy regimen comprising allogeneic stem cell transplantation. The method comprises administering allogeneic lymphocytes to the patient and monitoring the patient for levels of malignant cells.

Abstract: A biocompatible cell device having an internal foam scaffold to provide a growth surface for encapsulated cells which produce a biologically active molecule.

Abstract: The use of Tumor Cytotoxic Factor-II (TCF-II) enables the prevention and/or treatment of radiation-induced disorders.

Abstract: The present invention relates to a method by which one can target an undesired target molecule or target antigen, preferably a protein. The method comprises the intracellular expression of an antibody capable of binding to the target. A DNA sequence is delivered to a cell, the DNA sequence contains a sufficient number of nucleotides coding for the portion of an antibody capable of binding to the target operably linked to a promoter that will permit expression of the antibody in the cell(s) of interest. The antibody is then expressed intracellularly and binds to the target, thereby disrupting the target from its normal actions.

Abstract: The present invention provides a method of transplanting hematopoietic system reconstituting cells from a donor into an allogeneic recipient comprising administering to the recipient, prior to the administration of the hematopoietic system reconstituting cells, an amount of mononuclear cells which are treated so as to render them incapable of proliferating and causing a lethal graft versus host disease effect, but which are effective in enhancing subsequent engraftment of the hematopoietic system reconstituting cells in the recipient; and administering to the recipient an effective amount of hematopoietic system reconstituting cells.

Abstract: A method for inhibiting rejection by a recipient animal of a transplanted tissue, said method comprising modifying, eliminating, or masking an antigen which, when present on the surface of a cell of said tissue, is capable of causing a T-lymphocyte-mediated response in said animal, to inhibit antigen-mediated interaction between said cell and a T-lymphocyte of said animal without causing lysis of said cell.

Abstract: Laboratory non-human animals in which the immune system of a donor is induced in and thrives in vivo and expresses the immune response of the donor animal in a recipient non-human animal of a different species than the donor, and wherein malignant immune system cells of the donor can be induced in the recipient non-human animal by injection of non-malignant donor into the recipient are disclosed.