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13th International Congress on Autoimmunity, will be organized around the theme “Unveiling the versatile therapies to achieve breakthrough in Immunity”

Autoimmunity 2019 is comprised of keynote and speakers sessions on latest cutting edge research designed to offer comprehensive global discussions that address current issues in Autoimmunity 2019

Submit your abstract to any of the mentioned tracks.

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One of the functions of the immune system is to protect the body by responding to invading microorganisms, such as viruses or bacteria, by producing antibodies or sensitized lymphocytes (types of white blood cells). Under normal conditions, an immune response cannot be triggered against the cells of one's own body. In some cases, however, immune cells make a mistake and attack the very cells that they are meant to protect. This can lead to a variety of autoimmune diseases. They encompass a broad category of related diseases in which the person's immune system attacks his or her own tissue.
  • Track 1-1Achalasia
  • Track 1-2Addison’s disease
  • Track 1-3Lupus
  • Track 1-4Meniere’s disease
  • Track 1-5Narcolepsy

The study of the molecular and cellular components that comprise the immune system, including their function and interaction, is the central science of immunology. The immune system has been divided into a more primitive innate immune system and, in vertebrates, an acquired or adaptive immune system.


  • Track 2-1Malignant disease
  • Track 2-2Growing tumor
  • Track 2-3 Apoptosis
  • Track 2-4IgG1
Cancer immunology is division of biology which deals with understanding the role of the immune system in the development of cancer and string. The most well notable application in cancer immunology is cancer immunotherapy which taps the immune system as a treatment for cancer. Cancer immunologic surveillance and immune editing is based on immunity against development of automatic and chemically promote tumors in identification of targets animal systems and for immune recognition of human cancer.
  • Track 3-1Auto-immune Disease
  • Track 3-2Cancer
  • Track 3-3Malignancy
  • Track 3-4Rheumatic Disease
The principle of therapy for chronic inflammatory liver diseases is the removal of causal agents. For autoimmune liver diseases, however, total removal of causal agents and immune cells is impossible. Therefore, autoimmune liver diseases are presently treated by suppression of the immune response. Autoimmune hepatitis is characteristically responsive to corticosteroids, often used in combination with azathioprine to obtain a steroid-sparing effect. For primary biliary cirrhosis, ursodeoxycholic acid is safe and is the first choice for treatment. Treatment of this autoimmune liver disease should also address various symptoms and complications arising from any associated autoimmune diseases, particularly cholestasis and cirrhosis-related complications. For primary sclerosing cholangitis there are no established immunomodulatory therapies, but medical, endoscopic, and surgical treatments are applicable to this disease. Liver transplantation becomes indicated during the eventual end stages of each of these immune-mediated liver diseases.
  • Track 4-1Autoimmune cholangitis
  • Track 4-2Autoimmune liver Disease
  • Track 4-3Liver Transplantation
Cytokines which comprise of a family of proteins--interleukins, lymphokines, monokines, interferons, and chemokines, are important components of the immune system. They act in concert with specific cytokine inhibitors and soluble cytokine receptors to regulate the human immune response. Their physiologic role in inflammation and pathologic role in systemic inflammatory states are now well recognized. An imbalance in cytokine production or cytokine receptor expression and/or dysregulation of a cytokine process contributes to various pathological disorders. Research is progressing rapidly in the area of cytokines and their therapeutic targets, the two major therapeutic modalities being the administration of purified recombinant cytokines and the use of their antagonists in various inflammatory disorders. However, given the large number of cytokines, it is disappointing that only relatively few can be used clinically.
  • Track 5-1IL-1 Family
  • Track 5-2IL-1 Receptors
  • Track 5-3Interferon (IFN)
  • Track 5-4TGF beta Family
  • Track 5-5Chemokine & Chemokine Receptor

Autoimmunity results from a break in self-tolerance involving humoral and/or cell-mediated immune mechanisms. One pathological consequence of a failure in central and/or peripheral tolerance is the generation of autoantibodies and subsequent formation of complement-fixing immune complexes that contribute to tissue damage. Prevailing pharmacological strategies for treating autoimmune diseases involve the use of broad-acting immunosuppressants that with long term use have associated toxicities. The current drive in drug development is towards therapies that target a specific biological pathway or pathogenic cell population. Recent discovery of the BAFF-mediated B-cell survival pathway provides a unique opportunity for developing focused intervention for autoreactive B-cell function.

  • Track 6-1Drug Delivery Systems
  • Track 6-2Tumor Necrosis Factor-alpha/Metabolism
  • Track 6-3Membrane Proteins/Antagonists & Inhibitors

Self-tolerance loss is fundamental to autoimmunity. While understanding of immune regulation is expanding rapidly, the mechanisms causing loss of tolerance in most autoimmune diseases remain elusive. Autoimmunity is believed to develop when genetically predisposed individuals encounter environmental agents that trigger the disease. Recent advances in the genetic and environmental contributions to autoimmunity suggest that interactions between genetic elements and epigenetic changes caused by environmental agents may be responsible for inducing autoimmune disease.

  • Track 7-1Autoimmunity Genetics
  • Track 7-2Genetic Immunology
  • Track 7-3Genetic Predisposition to Disease
  • Track 7-4X Chromosome Inactivation
Virus infection is a primary factor that has been implicated in the initiation of autoimmune disease. Infection triggers a robust and usually well-coordinated immune response that is critical for viral clearance. However, in some instances, immune regulatory mechanisms may falter, culminating in the breakdown of self-tolerance, resulting in immune-mediated attack directed against both viral and self-antigens. Traditionally, cross-reactive T-cell recognition, known as molecular mimicry, as well as bystander T-cell activation, culminating in epitope spreading, have been the predominant mechanisms elucidated through which infection may culminate in an T-cell-mediated autoimmune response.
  • Track 8-1Desensitization
  • Track 8-2Immunologic
  • Track 8-3Immunologic Factors & therapeutic use
Translational immunology is the process by which researchers use immunological discoveries to develop practical solutions for human problems. Examples include the development of vaccines against infectious diseases or the engineering of new types of drugs to treat inflammatory disorders.



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  • Track 9-1Schizophrenia
  • Track 9-2MHC

The complement system is an ancient and evolutionary conserved element of the innate immune mechanism. It comprises of more than 20 serum proteins most of which are synthesized in the liver. These proteins are synthesized as inactive precursor proteins which are activated by appropriate stimuli. The activated forms of these proteins act as proteases and cleave other components successively in amplification pathways leading to exponential generation of final effectors. Three major pathways of complement pathways have been described, namely the classical, alternative and lectin pathways which are activated by different stimuli.

  • Track 10-1Adaptive Immunity
  • Track 10-2Complement Activation/Drug effects
  • Track 10-3Drug Evaluation, Preclinical
  • Track 10-4Complement Membrane Attack Complex
There is growing recognition in the scientific community that autoimmune diseases result from immunodeficiency, which disturbs the ability of the immune system to distinguish "self" from "non-self". The normalization of the immune system induced by LDN makes it an obvious candidate for a treatment plan in such diseases.The experience of people who have autoimmune diseases and who have begun LDN treatment has been remarkable. Patients with diagnoses such as systemic lupus, rheumatoid arthritis, Behcet's syndrome, Wegener's granulomatosis, bullous pemphigoid, psoriasis, and Crohn's disease have all benefited. Because LDN clearly halts progression in multiple sclerosis, its use has been more recently extended to other neurodegenerative diseases, such as Parkinson's disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) whose etiology remains unknown but for which there is suggestive evidence of a possible autoimmune mechanism.
  • Track 11-1Immunosuppressive Drugs
  • Track 11-2Ulcerative colitis
Forecast the outcome of therapy in clinical trials, or aid in developing improved treatments or preventative measures. All of these applications have been applied to the autoimmune diseases. As a case in point, we have through the years used biomarkers to predict susceptibility and the longer-range outcome of thyroid autoimmunity employing, a number of different approaches. They have taught us valuable lessons for future broader applications of biomarkers. The clues for susceptibility include major histocompatibility complex (MHC) and non-MHC genes combined with the fine specificity of thyroid autoantibodies in siblings of patients with juvenile thyroid disease. Together these biomarkers are highly predictive of later thyroid autoimmunity and subclinical thyroid dysfunction. For example, the progression from benign autoimmunity to clinical thyroid disease is marked by the appearance of autoantibodies to species-restricted epitopes on thyroglobulin. Thus, predictive biomarkers aid in identifying individuals with inordinate risk of disease and provide opportunities for earlier interventions to arrest the disease process.
  • Track 12-1Autoimmune Diseases Prevention & Control
  • Track 12-2Humans
  • Track 12-3Risk Factors
Biomarkers, represented by genetically determined traits or biologic changes predictive of disease onset or outcome, are increasingly employed by academic and industrial investigators. They can identify unusually susceptible populations or individuals, facilitate prognosis, Currently, autoimmune conditions are treated with immune suppressive agents such as steroids, methothrexate, cyclosporine, gold, and more recently infliximab (Remicade). Despite inducing temporary improvement, these approaches possess the possibility of long-term adverse effects, as well as need for life-long treatment.
Stem cell therapy has been demonstrated to induce profound healing activity in animals with various forms of autoimmune disorders. Besides healing damaged tissues, stem cells have the unique ability to modulate the immune system so as to shut off pathological responses while preserving its ability to fight off disease. Stem cells and specifically, mesenchymal stem cells home to inflamed tissue and start producing anti-inflammatory agents. These mediators act locally and do not suppress the immune response of the patient’s whole body. Additionally, mesenchymal stem cells induce the production of T regulatory cells, a type of immune cell whose function is to protect the body against immunological self-attack.
  • Track 13-1Hematopoietic Stem Cell Therapy for Autoimmune Diseases
  • Track 13-2Development of Hematopoietic Stem Cell Lines for Transplantation
  • Track 13-3Gene Therapy and Stem Cell Approaches for the Treatment of Autoimmune Diseases
Also called Hashimoto's disease, Hashimoto's thyroiditis is an autoimmune disease, a disorder in which the immune system turns against the body's own tissues. In people with Hashimoto's, the immune system attacks the thyroid. Located in the front of your neck, the thyroid gland makes hormones that control metabolism.
  • Track 14-1Multiple Sclerosis
  • Track 14-2Myxedema

Several self-molecules have been identified as target antigens in autoimmune diseases. Since lack or loss of tolerance to these molecules is one of the key events promoting autoimmunity, researchers are exploring the possibility that the administration of antigens or peptides may stimulate tolerogenic mechanisms and delay or prevent the full phenotypic expression of autoimmune diseases. There is much enthusiasm for such therapies, as these will probably be disease-specific and not associated with the side effects of conventional immunosuppression



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  • Track 15-1Thymus
  • Track 15-2Harnessing Treg cells
  • Track 15-3Designing Peptides for Therapy