Abstract: The inventors demonstrate that treatment of young, suckling mice with a glycolipid derived from Helicobacter pylori activates NKT cells in a CD1d-restricted fashion, and is protective against AHR in a model of allergen-induced asthma. The inventors further found that this protective effect can be transferred by NKT cells exposed to the glycolipid, and is associated with the expansion of a suppressive double-negative NKT cells and Foxp3+ TReg cells. The inventors also demonstrate herein that pre-treatment of adult mice with a glycolipid derived from Helicobacter pylori partially suppresses airway hyperreactivity and inhibits BAL inflammation in an ozone-exposure model. Accordingly, provided herein are compositions and methods for the treatment and prevention of inflammatory diseases, such as asthma or autoimmune diseases, in a subject in need thereof.

Abstract: A genetic locus and corresponding family of proteins associated with regulation of immune function and cell survival are provided. These genes encode cell surface molecules with conserved IgV and mucin domains. The locus comprising the TIM family is genetically associated with immune dysfunction, including asthma. Furthermore, the TIM gene family is located within a region of human chromosome 5 that is commonly deleted in malignancies and myelodysplastic syndrome. Polymorphisms in the gene sequences are associated with the development of airway hyperreactivity and allergic inflammation, and T cell production of IL-4 and IL-13. The proteins include the human hepatitis A cellular receptor, hHAVcr-1.

Abstract: Molecules that interact with the NKT cell antigen receptor and its counterpart antigen presenting molecule, but which inhibit the NKT cell immune function, are administered to a patient. Conditions of particular interest include the treatment of systemic lupus erythematosus (SLE), cancer, atherosclerosis, and allergic disease. In some embodiment of the invention, the inhibitory agent is an anergizing glycolipid, for example ?-galactosylceramide. Pharmaceutical formulations of such glycolipids are provided, and find use in the treatment of diseases involving undesirable NKT cell activation.

Abstract: A genetic locus and corresponding family of proteins associated with regulation of immune function and cell survival are provided. These genes encode cell surface molecules with conserved IgV and mucin domains. The locus comprising the TIM family is genetically associated with immune dysfunction, including asthma. Furthermore, the TIM gene family is located within a region of human chromosome 5 that is commonly deleted in malignancies and myelodysplastic syndrome. Polymorphisms in the gene sequences are associated with the development of airway hyperreactivity and allergic inflammation, and T cell production of IL-4 and IL-13. The proteins include the human hepatitis A cellular receptor, hHAVcr-1.

Abstract: The invention provides strategies for treating and preventing airway hyperreactivity and non-allergic asthma comprising antagonizing IL-17 activity and/or production by iNKT cells. Provided herein is a method of diagnosing non-allergic asthma and airway hyperreactivity comprising neutrophils quantification in sputum.

Abstract: A genetic locus and corresponding family of proteins associated with regulation of immune development, function, and cell survival are provided. The locus comprising the TIM family is genetically associated with immune dysfunction, including atopy, autoimmunity, inflammatory bowel disease, dysplasia, and susceptibility to blood-bourne infectious diseases. Polymorphisms in the human TIM-1 gene and exposure to Hepatitis A Virus (HAV) are shown to be associated with protection from the development of atopy.

Abstract: Molecules that interact with the NKT cell antigen receptor and its counterpart antigen presenting molecule, but which inhibit the NKT cell immune function, are administered to a patient. Conditions of particular interest include the treatment of systemic lupus erythematosus (SLE), cancer, atherosclerosis, and allergic disease. In some embodiment of the invention, the inhibitory agent is an anergizing glycolipid, for example ?-galactosylceramide. Pharmaceutical formulations of such glycolipids are provided, and find use in the treatment of diseases involving undesirable NKT cell activation.

Abstract: Molecules that interact with the NKT cell antigen receptor and its counterpart antigen presenting molecule, but which inhibit the NKT cell immune function, are administered to a patient. Conditions of particular interest include the treatment of systemic lupus erythematosus (SLE), cancer, atherosclerosis, and allergic disease. In some embodiment of the invention, the inhibitory agent is an anergizing glycolipid, for example ?-galactosylceramide. Pharmaceutical formulations of such glycolipids are provided, and find use in the treatment of diseases involving undesirable NKT cell activation.

Abstract: A genetic locus and corresponding family of proteins associated with regulation of immune function and cell survival are provided. These genes encode cell surface molecules with conserved IgV and mucin domains. The locus comprising the TIM family is genetically associated with immune dysfunction, including asthma. Furthermore, the TIM gene family is located within a region of human chromosome 5 that is commonly deleted in malignancies and myelodysplastic syndrome. Polymorphisms in the gene sequences are associated with the development of airway hyperreactivity and allergic inflammation, and T cell production of IL-4 and IL-13. The proteins include the human hepatitis A cellular receptor, hHAVcr-1.

Abstract: Methods are provided for the treatment of allergic and other immune disorders associated with overproduction of Th2 type cytokines by antigen specific T cells. Immunotherapy with adjuvants, as provided in the present invention, greatly inhibits the development of airway hyperreactivity and airway inflammation. Such immunotherapy is shown to reverse ongoing airway disease, and convert allergic inflammatory responses into protective immune responses. Conditions of particular interest include allergic conditions associated with production of Th2 cytokines and/or IgE antibodies, asthma, allergic rhinitis, and anaphylactic reactions. The addition of adjuvant induces a Th1-type immune response and can redirect an established Th2-type response to a Th1-type response for the selected antigen. Preferably, antigen-specific IgE production is reduced without altering the intensity of the antigen-specific proliferative response.

Abstract: A genetic locus and corresponding family of proteins associated with regulation of immune function and cell survival are provided. These genes encode cell surface molecules with conserved IgV and mucin domains. The locus comprising the TIM family is genetically associated with immune dysfunction, including asthma. Furthermore, the TIM gene family is located within a region of human chromosome 5 that is commonly deleted in malignancies and myelodysplastic syndrome. Polymorphisms in the gene sequences are associated with the development of airway hyperreactivity and allergic inflammation, and T cell production of IL-4 and IL-13. The proteins include the human hepatitis A cellular receptor, hHAVcr-1.

Abstract: Methods are provided for the treatment of allergic and other immune disorders associated with overproduction of Th2 type cytokines by antigen specific T cells. Immunotherapy with adjuvants, as provided in the present invention, greatly inhibits the development of airway hyperreactivity and airway inflammation. Such immunotherapy is shown to reverse ongoing airway disease, and convert allergic inflammatory responses into protective immune responses. Conditions of particular interest include allergic conditions associated with production of Th2 cytokines and/or IgE antibodies, asthma, allergic rhinitis, and anaphylactic reactions. The addition of adjuvant induces a Th1-type immune response and can redirect an established Th2-type response to a Th1-type response for the selected antigen. Preferably, antigen-specific IgE production is reduced without altering the intensity of the antigen-specific proliferative response.