Abstract: Described herein is a treatment comprising the following step: (a) injecting a therapeutically effective amount of a pharmaceutical composition into the celiac artery of an individual, wherein the pharmaceutical composition reverses recent onset Type 1 Diabetes (T1D). Also described is a method for identifying an individual who will be responsive to this treatment. In addition there is described a device containing the pharmaceutical composition for injecting the pharmaceutical composition into the celiac artery.

Abstract: Described herein is a treatment comprising the following step: (a) injecting a therapeutically effective amount of a pharmaceutical composition into the celiac artery of an individual, wherein the pharmaceutical composition reverses recent onset Type 1 Diabetes (T1D). Also described is a method for identifying an individual who will be responsive to this treatment. In addition there is described a device containing the pharmaceutical composition for injecting the pharmaceutical composition into the celiac artery.

Abstract: Described herein is a treatment comprising the following step: (a) injecting a therapeutically effective amount of a pharmaceutical composition into the celiac artery of an individual, wherein the pharmaceutical composition reverses recent onset Type 1 Diabetes (T1D). Also described is a method for identifying an individual who will be responsive to this treatment. In addition there is described a device containing the pharmaceutical composition for injecting the pharmaceutical composition into the celiac artery.

Abstract: Described herein is a treatment comprising the following step: (a) injecting a therapeutically effective amount of a pharmaceutical composition into the celiac artery of an individual, wherein the pharmaceutical composition reverses recent onset Type 1 Diabetes (T1D). Also described is a method for identifying an individual who will be responsive to this treatment. In addition there is described a device containing the pharmaceutical composition for injecting the pharmaceutical composition into the celiac artery.

Abstract: Described herein is a treatment comprising the following step: (a) injecting a therapeutically effective amount of a pharmaceutical composition into the celiac artery of an individual, wherein the pharmaceutical composition reverses recent onset Type 1 Diabetes (T1D). Also described is a method for identifying an individual who will be responsive to this treatment. In addition there is described a device containing the pharmaceutical composition for injecting the pharmaceutical composition into the celiac artery.

Abstract: Methods for the treatment, inhibition, prevention, etc. of metabolic syndrome (MetSyn) and/or Type-2 diabetes (T2D) using a T cell activating antibody that stimulates activation and immunomodulation of T-cells to affect the immune environment of adipose tissue and improve insulin sensitivity. Also methods for the treatment, inhibition, prevention, amelioration, reversal, etc., of metabolic syndrome (MetSyn) and/or Type-2 diabetes (T2D) using leukemia inhibitory factor (LIF), or a functional portion thereof. Compositions administered to individuals having or at risk of developing MetSyn and/or T2D may include pharmaceutical compositions. Methods may also provide tolerogenic vaccines based on the administration of identified auto-antigens from individuals having or at risk of developing MetSyn and/or T2D.

Abstract: The present invention provides a method of altering the function of TRPV1+ sensory afferent neurons in the pancreas as a way of treating, managing, alleviating, etc., the symptoms and/or underlying causes of diabetes or abnormal glucose metabolism by increasing the release of neuropeptides, such as substance P (sP) or other tachykinin peptide, in the pancreas. This may be achieved by injecting a TRPV1 agonist, such as a capsaicinoid compound or capsaicin analog, or a neuropeptide, such as sP or other tachykinin peptide, directly into the pancreas, or alternatively, by stimulating one or more intercostal and/or subcostal nerves of spinal nerves derived from one or more thoracic segments T8 through T12 by chemical, electrical, surgical, mechanical, etc., methods.

Abstract: A process is disclosed for controlling inflammatory tissue access through release of neuropeptides, such as substance P (sP), to insulin-responsive sensory neurons, whereby simultaneous control of insulin sensitivity/resistance is manifested. In models of Type 1 and Type 2 diabetes, sensory afferents, in particular TRPV1, have fundamental roles in insulin/glucose homeostasis, islet physiology and autoimmune tissue inflammation. By manipulation of the TRPV1 neuro-?-cell circuit or enhancement of pancreatic sP levels, normalization of insulin resistance, clearance of inflammation and prevention of both Type 1 and Type 2 diabetes is realized.

Abstract: A process is disclosed for controlling inflammatory tissue access through release of neuropeptides, such as substance P (sP), to insulin-responsive sensory neurons, whereby simultaneous control of insulin sensitivity/resistance is manifested. In models of Type 1 and Type 2 diabetes, sensory afferents, in particular TRPV1, have fundamental roles in insulin/glucose homeostasis, islet physiology and autoimmune tissue inflammation. By manipulation of the TRPV1 neuro-?-cell circuit or enhancement of pancreatic sP levels, normalization of insulin resistance, clearance of inflammation and prevention of both Type 1 and Type 2 diabetes is realized.

Abstract: A process is disclosed for controlling inflammatory tissue access through release of neuropeptides, such as substance P (sP), to insulin-responsive sensory neurons, whereby simultaneous control of insulin sensitivity/resistance is manifested. In models of Type 1 and Type 2 diabetes, sensory afferents, in particular TRPV1, have fundamental roles in insulin/glucose homeostasis, islet physiology and autoimmune tissue inflammation. By manipulation of the TRPV1 neuro-?-cell circuit or enhancement of pancreatic sP levels, normalization of insulin resistance, clearance of inflammation and prevention of both Type 1 and Type 2 diabetes is realized.

Abstract: This invention relates to identification of an autoantigen implicated in the development and progression of Sjögren's Syndrome (pSS); particularly to the disease modifying effect of creating a deficiency in the ICA69 autoantigen; and most particularly to development of diagnostic and therapeutic avenues, means for the differential diagnosis of pSS versus other autoimmune disease, e.g. Systemic lupus erythematosis (SLE), and procedures for immunotherapeutic treatment effective to alter the course and progression of pSS.

Abstract: This invention relates to identification of an autoantigen implicated in the development and progression of Sjögren's Syndrome (pSS); particularly to the disease modifying effect of creating a deficiency in the ICA69 autoantigen; and most particularly to development of diagnostic and therapeutic avenues, means for the differential diagnosis of pSS versus other autoimmune disease, e.g. Systemic lupus erythematosis (SLE), and procedures for immunotherapeutic treatment effective to alter the course and progression of pSS.

Abstract: This invention relates to identification of an autoantigen implicated in the development and progression of Sjögren's Syndrome (pSS); particularly to the disease modifying effect of creating a deficiency in the ICA69 autoantigen; and most particularly to development of diagnostic and therapeutic avenues, means for the differential diagnosis of pSS versus other autoimmune disease, e.g. Systemic lupus erythematosis (SLE), and procedures for immunotherapeutic treatment effective to alter the course and progression of pSS.

Abstract: Methods and compositions are provided for preventing the development of a T cell mediated autoimmune disease such as Type I diabetes, in which susceptible subjects have T cells sensitized to a disease-related antigen. Subjects are treated by administration of the antigen or fragments thereof to prevent the expansion of the population of sensitized T cells. Alternatively, subjects are treated by administration of immunogenic compositions comprising a mimicry antigen or fragments thereof.