[AUTOIMMUNITY] July 14, 2013

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1 This sheet includes only the extra notes. Slide 5,6: [AUTOIMMUNITY] July 14, 2013 Autoimmunity is the condition or case where the immune system is activated by self antigensand when the immune system no longer recognizes itself which is the most important characteristic of the adaptive immune system self-nonself discrimination. And generally self tolerance is acquired, where self reactive antigens are eliminated, ( self reactive antigens here refer to B or T cell receptors on B or T lymphocytes. So, our body cannot eliminate all the self reactive antigens because some of these help in protecting us from foreign antigens, so its impossible to remove all autoreactive B or T lymphocytes from the body. The simplest reason is the inability to present all self antigens to B or T lymphocytes during maturation. Those B or T lymphocytes carrying a receptor that react with hidden nonpresentedself antigens will be present in the immune repertoire. This means that everyone has some self reactive antigens that are not activated. As we talked in the last lecture, individuals inherit the genes that enable them to mount a response against self. But this is regulated at the phenotypic level.so genetically T and B lymphocytes are self reactive, however those that are detected as self reacting are eliminated in the thymus or the bone more. Slide 7 :

2 We should distinct between autoimmune response and autoimmune disease.autoimmune response involves interaction with cells but may not be associated with pathology. But, autoimmune diseases are those autoimmune responses that develop in pathologic conditions. Without autoimmune responses, the immune system wont function normally. Its very essential for the interaction between CD molecules ( CD4, CD8 ) and MHC, they are also essential for the regulation of the immune system thatidiotypeantiidiotype responses develop. Slide 8 : So we can introduce two terms : - Normal autoimmunity - Autoimmune diseases. Normal autoimmunity doesn t indicate failure of tolerance induction, especially tolerance at the central level as the body exerts extra precautions to maintain tolerance. Slide 9 : Titer < 4 is present in all healthy individuals. Natural autoantibodies can bind to intracellular constituents, ( the released ones as a result of cell death ). Slide 11 : Its believed that autoantibodies can prevent autoimmune diseases by blinding the immune system of these self components that are released as a result of cell death for example.so these autoantibodies will bind to them and they will be cleared by phagocytosis, but if they for a long

3 period of time, this will trigger an adaptive immune response against these autoantibodies. Myasthenia graves antibodies against acetylcoline receptors which block the binding acetylcolineto its receptor in postsynaptic site and this will decreaseor block the contractility of the muscles that is associated with sever muscle pain. The acetyl colinereceptors are of IgGclass,and pregnant woman with myasthenia graves will provide these antibodies to their fetus, so the antibody passes to the placenta, crosses it and reaches the circulation. New born are born with manifestations of myasthenia graves, but these manifestations will decrease with time and by the 6 months they are gone due to the normal decay of immuneglobulin without any treatment. Slide 12 : Autoimmune diseases are very common. Common by percentage is defined as 1%. Slide 13 : Autoimmune diseases should be distinguished from the conditions where an antibody or a cell mediated immunity develops causing tissue damage but the trigger is not self antigens. We have cases like infections, for ex. TB, associated with immune mediated tissue damage but the trigger is not self antigens. Animal models like these which are available for the study of multiple sclerosis, mice for the study of experimental allergic encephalitis.

4 Slide 14,15 : From the figure we can conclude that autoimmune diseases are multifactorial notsingle. Autoimmunity is of many mechanisms that are clear: Failure of tolerance induction :its not common, especially at the central level, its difficult to break a T cell tolerance but the B cell tolerance is easier to break. CTLA-4 :cytotoxic T lymphocyte antigen 4, binds to the CD8. Apoptosis of T lymphocytes results as a result of the expression of fasligand. Excess IL2, especially at the B cell level, the injection of increased amounts of IL2 can break tolerance. Antigens that are hidden from the immune system are regarded as nonself (not sure, check it at 19:54), because the immune system is educated to recognize self, if these antigens can be brought to the thymus or the bone marrow they will be recognized as self, but if not, they will be recognized as foreign. Neoantigens can stimulate immune system. In Multiple sclerosis, T lymphocytes act as the effector, they recognize myelin as foreign, in infection, the exposure of this myelin will cause attack of these myelin sheaths by T lymphocytes,and those that attack myelin sheaths will expose more myelin, so more spreading. Its believed that conformational change is responsible for the production of IgM antibodies against the Fc fragment of IgG which is believed to be the rheumatic factor.

5 Slide 16: Cryptic epitopes can be exposed by break down of barriers like blood testis barrier, vasectomy exposes sperms and this will cause production of antispermantiobodies and infertility can develop because sperms are hidden by barriers from immune system, Molecular mimicry is the presence of cross reacting antigens in substances on the surface of organisms, that cross react with antigens on the tissues. Like in rheumatic fever where strep. M protein cross react with antigens on sarcolemmal membrane and valves. And antibodies produced against M protein will bind to antigens on the sarcolemmal membrane and valves and activate rheumatic fever. -Insulin dependant diabetes millets : Where coxsakie and cmv antigens cross react with Glutamin Acid Decarboxylase (GAD) on B-cells of pancrease. -T Helper 1-T Helper 2 balance associated with establishment of tolerance. Its imbalanced when associated with autoimmunity. _superantigens can activate multiple clones of T-lymphocytes by binding to the variable domain of the B chain of TCR. Slide 18:

6 -Smoking can cause damage to the basement membrane of the alveoli, this will expose collagen 4 which will be recognized as foreign because it was not introduced during the development of T-cells, this will lead to the production of antibodies against collagen 4, this is followed by the formation of complexes between antibodies and the basement membrane of the lung and the kidney, so good pastures syndrome involves the lung and the kidney, leading to hemoptysis( coughing of blood) in the lung, and glomerulonephritis in the kidney. -EAE: experimental allergic encephalitis -The best example of an injury that can trigger an immune response is eye trauma, 'cause it releases tissue of the eye lens which is considered sequestered antigens, so an immune response can develop, leading to opthalmitis. Slide 19: Immune stimulation is another mechanism for development of an auto immune response. -there are some tissues that do not express MHC whether class 1 or 2, IFNγ can increase the expression of MHC I and II, it is produced in high concentrations in infections or inflammation, so it will increase the expression of MHC II by tissues, for example by thyroid tissue. Thyroid tissue will be regarded as foreign, this will lead to auto immune thyroiditis.

7 -MHC cannot be expressed unless loaded with a peptide, this peptide will be derived from thyroid cells, and so this will lead to an auto immune thyroiditis. Slide 20: -In graves disease the TSH receptor is recognized as foreign, and antibodies produced against this TSH receptor can bind to it. -Thyroid hormones will inhibit the synthesis of further TSH,feed back inhibition. -naturally increased production of hormones will inhibit further production of TSH, but in graves the receptors are occupied and saturated by the auto antibodies, leading to production of thyroid hormones and more TSH will be produced as well, leading to thyrotoxicosis. so this disease is associated with hyper reactivity of the thyroid gland. Slide 21 : Naturally TSH binds to TSH receptors in the thyroid gland and stimulate the production of thyroid hormones, then the thyroid hormone inhibit further production of TSH by feedback inhibition. In grave s disease the antibody mimic the action of the normal TSH causing increase production of thyroid hormones. The hormones will inhibit the further production of TSH, but in this case the TSH can t suppress the production of the hormones because the receptors are

8 saturated by antibodies and that cause increase the level of thyroid hormones which will cause thyrotoxicosis. Slide : Naturally,activation of T cells will lead to expression of Fas(CD95)and Fas ligand bind to this molecule causing cell death and apoptosis. In cases of defective expression of these ligands will cause to cell survive and mutation in Fas/ Fas ligands and lead to what we called AIPS. TCR double negative present in circulation in very low amount but in ALPS they increase in number. Slide 25 : Transforming growth factor beta (TGF-beta)and IL-6 cause the development of Th17 and Th17 produce IL17. Mice that lack IL17 don t develop Experimental Allergic encephalitis which is equivalent to multiple sclerosis. That means IL17 mediate multiple sclerosis. Slide 26 : Intrinsic factor is important in absorption of vitamin b12 and its produced from parietal cells of GI tract and bind to B12 allowing its absorption. In certain conditions the IF recognized as foreign and antibody produced against it. Antibody make complexes with IF inhibiting its

9 binding to B12 so that B12 deficiency developed in condition known as pernicious anemia. Slide 27 : Characteristic of autoimmune disease 1-Systemic vs organ-specific In systemic the antigen stimulus will be common to all tissue Generally,its antibody mediated (not in all cases) In organ specific antigen stimulus will be specific to one tissue. Generally, its T cell mediated (not for all ) 2-Variable course within the same disease/ same individual Or different disease/ different individual. 3-Female preponderance (the exception is diabetes ) all autoimmune more common in female. The ratio could be 50:1 like in hashimoto. 4-Overlapping manifestations : because of similar immune pathology. 5-Diverse Immunopathology :it may be mediated by antibody or immune complex or T cells ( T helper or T cytotoxic ). 6-Immunosuppression : despite the fact is that an individual produces antibodies in high amounts against self antigens, when he s immunized with a foreign antigen he responses in proper ( suboptimal ) so they are immunosuppresent. 7-Constant antigen: the same antigen that trigger the autoimmune disease is the same in all individual in the same disease.

10 8-Genetic susceptibility: individual that inherit specific gene has higher risk to develop autoimmune disease. 9-Environmental factors such as drugs, infections and food all of them involved in autoimmune disease. Slide 29 : They found that left handed individual has higher risk to develop autoimmune disease. Slide 30 : Hashimoto disease : thyroglobulin is involved in the synthesis of T4,T3 hormones. inhibition of the hormone release will cause the pituitary gland to secrete more TSH and this is associated with the tissue response but failure to release the hormone so that an enlargement of the thyroid gland will result. (Goiter) Pancreas : more than one mechanism, insulin receptors, insulin itself. Slide 31 : SLE : antibodies produced against intracellular components, nuclear factors especially the double stranded DNA. These antigens antibody complexes will deposit everywhere in the body, ( heart, kidney, joints) and activate the complement that s why manifestations are multiple in SLE. Slide 32 : This skin manifestation as butterfly. Slide 33 :

11 All rheumatic diseases are autoimmune caused by different variable antigens most of them are proteins ( intracellular components ) Slide 36 : In hashimoto, antibodies block the function. Slide 38 : In APS-1 : decreased expression of self antigens will result in defect in negative selection, that means that auto reactive T lymphocytes will pass through. Slide 39,40 : If we assume to take diabetes, if we assume that genetics is not involved, there s no genetic susceptibility, and no genetic predisposition for diabetes. Then the distribution of HLA among diabetics will be equal.so, if we take 1000 thousand diabetics, ¼ of them will share 0 HLA and ¼ will share 2 HLA and 50% will share 1 HLA within a family, but what was detected is an increase in the rate of HLA sharing with diabetes. Slide 42 : The relative risk indicates the risk of acquiring the disease if you the gene in comparison with those who lack. Slide 43 : Prevalence of diabetes increases with the presence of both DR3 and DR4, but less than.5 with one of them and DR2. The risk is almost zero when the person is homozygous for DR2.

12 So, DR3 and DR4 predispose for diabetes but DR2 protects from it. Slide 49 : Certain molecules of TCR are associated with multiple sclerosis, antibodies to those molecules can treat MS. Special thanks for RouwandAbdulwahed and SaifAlHamaideh. By LinaBaker.

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