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Nbva9xnwtzky8uc2jiri 171207 s0 arfeen zain autoimmunity intro
05:03
Autoimmunity
Qmly5jkbqeu6uienwzcc 171207 s1 arfeen zain organ specific immune diseases
14:20
Organ Specific Immune Diseases
Bpiraxbarmvbzkmuhfoq 171207 s2 arfeen zain systemic autoimmune diseases and animal models
14:35
Systemic Autoimmune Diseases and Animal Models
3evvvphq6uqdqnoe4u6i 171207 s3 arfeen zain the cd4 t cell mhc and tcr in autoimmunity
11:05
The CD4+ T-Cell, MHC and TCR in Autoimmunity
Miwudsnutxctnynsqvbh 171207 s4 arfeen zain mechanisms for induction of autoimmunity
11:53
Mechanisms for Induction of Autoimmunity
Blsugvrstcjf9uk0owkk 171207 s5 arfeen zain treatment of autoimmune diseases
12:26
Treatment of Autoimmune Diseases

Lecture´s Description

Organ Specific Immune Diseases

In this lecture the educator explains about Autoimmunity. The section one consists of Autoimmune Diseases Due to Cellular Damage, Autoimmune Anemias and Diseases by Stimulating or Blocking Auto-Abs. Autoimmunity, can cause many chronic debilitating diseases. The symptoms of autoimmunity differ depending on which tissues and organs are under attack. For example, multiple sclerosis is due to an autoimmune attack on the brain and central nervous system, Crohn’s disease is an attack on the tissues in the gut, and rheumatoid arthritis is an attack on joints of the arms and legs. The genetic and environmental factors that trigger and sustain autoimmune disease are very active areas of immunologic research, as is the search for improved treatments. Autoimmunity, the state in which the immune system reacts against the body’s own normal components, producing disease or functional changes. The human immune system performs a surveillance function, identifying and disposing of antigens—materials such as toxins or infectious microbes that it recognizes as foreign. This surveillance is carried out mostly by the white blood cells called lymphocytes, which recognize foreign antigens and either attack them directly or produce antibodies against them.

Systemic Autoimmune Diseases and Animal Models

In section two the educator explains about SLE, MS and RA, Animal Models for Autoimmune Diseases and Spontaneous and Experimental Autoimmunity. Systemic lupus erythematosus (SLE), also known as lupus, is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body. Systemic lupus erythematosus (SLE), also known simply as lupus, is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body. Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord (central nervous system). In MS, the immune system attacks the protective sheath (myelin) that covers nerve fibres and causes communication problems between your brain and the rest of your body. Eventually, the disease can cause the nerves themselves to deteriorate or become permanently damaged. Signs and symptoms of MS vary widely and depend on the amount of nerve damage and which nerves are affected. Some people with severe MS may lose the ability to walk independently or at all, while others may experience long periods of remission without any new symptoms. There’s no cure for multiple sclerosis. However, treatments can help speed recovery from attacks, modify the course of the disease and manage symptoms. Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints. Autoimmune diseases are illnesses that occur when the body's tissues are mistakenly attacked by their own immune system.

The CD4+ T Cell, MHC, and TCR in Autoimmunity

Role of CD4+ T Cells and TH1/TH2 Balance and Autoimmunity due to MHC or TCRs is explained in section three. The inappropriate response to self-antigens that characterizes all autoimmune diseases can involve either the humoral or cell-mediated branches of the immune system. Identifying the defects underlying human autoimmune diseases has been difficult; more success has been achieved in characterizing the immune defects in the various animal models. Each of the animal models has implicated the CD4+ T cell as the primary mediator of autoimmune disease. For example, the evidence is quite strong that, in mice, EAE is caused by CD4+ TH1 cells specific for the immunizing antigen. The disease can be transferred from one animal into another by T cells from animals immunized with either MBP or PLP or by cloned T-cell lines from such animals. It also has been shown that disease can be prevented by treating animals with anti-CD4 antibodies. These data are compelling evidence for the involvement of CD4 in the establishment of EAE.T-cell recognition of antigen, of course, involves a trimol-ecular complex of the T-cell receptor, an MHC molecule, and antigenic peptide. Thus, an individual susceptible to autoimmunity must possess MHC molecules and T-cell receptors capable of binding self-antigens.

Mechanisms for Induction of Autoimmunity

In section four the educator Activation and clonal expansion of autoreactive lymphocytes is a critical step in the pathogenesis of autoimmune diseases. In experimental models of autoimmunity, disease can be transferred by activated, but not resting, autoreactive T cells (1), indicating that activation of autoreactive T cells is required for the development of autoimmune diseases. Infectious agents have long been considered as possible culprits in the activation of autoreactive T cells. Mechanisms by which an infection can lead to an autoimmune process have been examined in experimental animal models. Mechanisms for the induction of autoimmunity by infectious agents. Activation and clonal expansion of autoreactive lymphocytes is a critical step in the pathogenesis of autoimmune diseases. Inappropriate" expression of class II major histocompatibility complex (MHC) molecules by target cells has been found in all organ-specific autoimmune diseases so far examined for the presence of this phenomenon. These glycoproteins may have a functional role as class II+ thyrocytes are able to present both small fragments of foreign antigens and autoantigens to helper T cells. Interferon gamma is a likely modulator of MHC class II expression in the thyroid but other signals like thyroid-stimulating hormone seem to influence its action. By contrast, it appears that lymphokines are not involved in inducing the inappropriate MHC class II expression observed in situ in the pancreatic beta cells of diabetics.

Treatment of Autoimmune Diseases

In section five the educator explains about Treatment of Autoimmune Diseases, Novel Targets for Treatment and T-Cell Vaccination Is a Possible Therapy. Types of treatments include: Supplements to replace a substance that the body lacks, such as thyroid hormone, vitamin B12, or insulin, due to the autoimmune disease. Blood transfusions if blood is affected. Physical therapy to help with movement if the bones, joints, or muscles are affected. Autoreactive T-cells are regulated under the normal conditions and play an important role in autoimmune pathologies when they are dysregulated because of genetic, environmental and other unknown factors associated with various autoimmune diseases. The immune regulation of autoreactive T-cells may be regained by activating the regulatory network, such as the idiotype anti-idiotypic network. Immunization with inactivated autoreactive T-cells (T-cell vaccination) can be used as a powerful means of activating the idiotype anti-idiotypic network to deplete specific subsets of autoreactive T-cells potentially involved in autoimmune conditions. It induces regulatory immune responses that closely resemble the in vivo situation, where the immune system is challenged by clonal activation and expansion of given T-cell populations in various autoimmune diseases. Recent clinical trials in multiple sclerosis have begun to reveal the role of T-cell vaccination in the understanding of in vivo regulation of autoreactive T-cells and in the development of effective therapeutic strategies for multiple sclerosis and other autoimmune conditions.

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