Autoimmunity refers to an aberration in the body's normal development such that the immune system mounts an attack against its own cells.

Autoimmunity is the system of immune responses of an organism against its own healthy cells, tissues, and other normal body constituents. Any disease resulting from this type of immune response is termed an "autoimmune disease.".

1. AUTOIMMUNITY & DISEASES DEPARTMENT OF MICROBIOLOGY AYUSHI SHARMA

2. AUTOIMMUNITY Autoimmunity is the failure of an organism in recognizing its own constituent parts as self , thus leading to an immune response against its own cells and tissues .   Autoimmune diseases are the consequence of an inappropriate immune response directed to self-antigens of healthy tissues. Any disease that results from such an aberrant immune response is termed as auto immune diseases.

3. CAUSES The cause of autoimmune diseases is unknown. If you have a family member with an autoimmune disease, you may be more susceptible to developing one. bacteria or virus drugs chemical irritants environmental irritants

4. TYPES Autoimmune diseases are of two types: Organ specific autoimmune diseases. 2. Systemic autoimmune diseases.

5. ORGAN SPECIFIC AUTOIMMUNE DISEASES An organ-specific disease is one in which an immune response is directed toward antigens in a single  organ or gland. Examples : Autoimmune anaemias Good pasteur’s syndrome Insulin dependent diabetes mellitus Grave’s disease Myasthenia gravis.

6. SYSTEMIC AUTOIMMUNE DISEASES A systemic autoimmune disease is that in which the targeted antigens are located throughout the body. Examples: Systemic lupus erythematosus Multiple sclerosis Rheumatoid arthritis.

7. AUTOIMMUNE ANAEMIAS Autoimmune anaemias include: 1. Pernicious anaemia 2. Hemolytic anaemia 3.Drug-induced hemolytic anaemia.

8. HEMOLYTIC ANAEMIA It occurs when auto- antibodies are directed against the antigens of person's own red blood cells (RBCs). Triggers complement mediated lysis or antibody mediated opsonization and phagocytosis of the red blood cells.

9. CAUSES  Blood disorders toxins infection by various bacteria and viruses

10. SYMPTOMS paleness of the skin fatigue fever confusion lightheadedness dizziness weakness/inability to do physical activity

11. TREATMENT blood transfusion intravenous immune globulin corticosteroid medication surgery

12. PERNICIOUS ANAEMIA Develops due to production of auto-antibodies against intrinsic factor which is a membrane bound intestinal protein on gastric parietal cells. Intrinsic factor facilitates uptake of vitamin B12 from small intestine which is necessary for hematopoiesis. Binding of auto-antibody to intrinsic factor mediated absorption of vitamin B12 resulting in reduction of number of mature red blood cells below normal.

13. CAUSES long-term use of certain medications and antibiotics (methotrexate, azathioprine, etc.) chronic obstructive pulmonary disease (COPD) folate deficiency caused by poor intake or malabsorption

14. SYMPTOMS weakness headaches chest pain weight loss unsteady gait Spasticity (stiffness and tightness in the muscles) peripheral neuropathy (damage to the nerves in your arms and legs) progressive lesions of the spinal cord memory loss

15. TREATMENT Vitamin B-12 injections that are slowly decreased over time Blood test for iron deficiency followed by regular blood tests CBC tests to measure serum cobalamin and ferritin levels Blood tests to monitor replacement treatments

16. GOOD PASTEUR’S SYNDROME   occurs when the body’s immune system mistakenly produce auto-antibodies against a protein called collagen in the alveoli of the lungs and the filtering units (glomeruli) of the kidney. Damage to glomerular and alveolar basement membranes leads to progressive kidney damage and pulmonary hemorrhage.

17. CAUSES Exposure to hydrocarbon fumes, metallic dust, tobacco smoke, or certain illegal substances such as cocaine may also increase risk.

18. SYMPTOMS fatigue, weakness, or lethargy nausea and/or vomiting loss of appetite unhealthy, pale appearance dry cough or coughing up blood shortness of breath or difficult breathing burning sensation during urination blood in the urine or foamy urine swelling of the hands and feet high blood pressure back pain below the ribs

19. TREATMENT immunosuppressive drugs  to keep immune system from making the antibodies that damage lungs and kidneys. Cyclophosphamide is one example. corticosteroids  like prednisone help control bleeding in lungs. These medications also suppress immune system.

20. INSULIN DEPENDENT DIABETES MELLITUS It  is a form of diabetes mellitus that results from the autoimmune destruction of the  insulin-producing beta cells in islets of langerhans of pancreas.  This results in lack of insulin leading to increased blood and urine glucose.

21. SYMPTOMS  polyuria (frequent urination)  polydipsia(increased thirst) xerostomia (dry mouth)  polyphagia (increased hunger) fatigue weight loss.

22. TREATMENT Taking insulin Exercising regularly and maintaining a healthy weight Eating healthy foods Monitoring blood sugar

23. GRAVE’S DISEASE It occurs due to an abnormal immune system response that causes the thyroid gland to produce too much thyroid hormone.  mediated by binding of auto antibodies on TSH receptor present on thyroid gland, activating adenylate cyclase resulting in production of thyroid hormones.

24. SYMPTOMS Anxiety Difficulty concentrating Double vision Eyeballs that stick out ( exophthalmos ) Eye irritation and tearing Fatigue Frequent bowel movements Goiter  (possible) Heat intolerance

25. SYMPTOMS Increased sweating Insomnia Irregular menstrual periods in women Muscle weakness Nervousness Rapid or irregular heartbeat (palpitations or arrhythmia) Restlessness and difficulty sleeping Shortness of breath with activity Tremor Weight loss(rarely, weight gain) Increases appetite

26. TREATMENT Radioactive iodine therapy Anti-thyroid medications Beta blockers Surgery

27. MYASTHENIA GRAVIS   A neuromuscular disease in which the muscles under our voluntary control become easily tired and weak because there is a problem with how the nerves stimulate the contraction of muscles.   circulating antibodies cause weakness by blocking acetylcholine receptors on motor end plates of muscles, blocking normal binding of acetylcholine.

28. SYMPTOMS  fatigue ptosis (drooping of one or both eyelids)  diplopia (double vision) blurred vision (which may be intermittent)  speech may become soft or nasal. making eating, drinking, swallowing pills harder. develop an unusual or different smile if certain facial muscles are affected.

29. SYMPTOMS   arm and leg muscles may weaken, affecting such activities as lifting or walking .

30. TREATMENT Anticholinesterase agents which improve neuromuscular transmission and muscle strength. Immunosuppressive drugs which suppress production of abnormal antibodies.

31. Antigen Presenting Cells (The Antigen Processing and Presentation) Foreign Pathogen protein antigen are degraded into small antigenic peptides that from complexes with class I or Class II MHC Molecule. The Conversion of Proteins into MHC associate Peptide fragments is called APC

32. APCs This can process a Protein antigen, break into peptides and Present it with class I and Class II molecule on cell surface where it way Interact with appropriate T Cell Receptors. They Engulf a a pathogen through phagocytosis and Presenting it to the Whole Immune Syatem . So, That Cell Mediated and Humoral Immune Response Can build Up. Some Examples of APC are- Dendritic Cell, Macrophages and B cell.

33. Role Of APCs Phagocytosis of Antigen Fusion of Lysosome and Phagosome Enzymes start to degrade Antigen Fragments of Ag presented on APC surface. Leftover fragments released by Exocytosis .

34. Unlike NK cells of the innate immune system, B cells (B lymphocytes) are a type of white blood cell that gives rise to antibodies, whereas T cells (T lymphocytes) are a type of white blood cell that plays an important role in the immune response. T cells are a key component in the cell-mediated response—the specific immune response that utilizes T cells to neutralize cells that have been infected with viruses and certain bacteria. There are three types of T cells: cytotoxic , helper, and suppressor T cells. Cytotoxic T cells destroy virus-infected cells in the cell-mediated immune response, and helper T cells play a part in activating both the antibody and the cell-mediated immune responses. Suppressor T cells deactivate T cells and B cells when needed, and thus prevent the immune response from becoming too intense. An  antigen  is a foreign or “non-self” macromolecule that reacts with cells of the immune system. Not all antigens will provoke a response. For instance, individuals produce innumerable “self” antigens and are constantly exposed to harmless foreign antigens, such as food proteins, pollen, or dust components. The suppression of immune responses to harmless macromolecules is highly regulated and typically prevents processes that could be damaging to the host, known as tolerance

35. APCs The innate immune system contains cells that detect potentially harmful antigens, and then inform the adaptive immune response about the presence of these antigens. An  antigen-presenting cell (APC)  is an immune cell that detects, engulfs, and informs the adaptive immune response about an infection. When a pathogen is detected, these APCs will phagocytose the pathogen and digest it to form many different fragments of the antigen. Antigen fragments will then be transported to the surface of the APC, where they will serve as an indicator to other immune cells.  Dendritic cells  are immune cells that process antigen material; they are present in the skin ( Langerhans cells) and the lining of the nose, lungs, stomach, and intestines. Sometimes a dendritic cell presents on the surface of other cells to induce an immune response, thus functioning as an antigen-presenting cell. Macrophages also function as APCs. Before activation and differentiation, B cells can also function as APCs. After phagocytosis by APCs, the phagocytic vesicle fuses with an intracellular lysosome forming phagolysosome . Within the phagolysosome , the components are broken down into fragments; the fragments are then loaded onto MHC class I or MHC class II molecules and are transported to the cell surface for antigen presentation, as illustrated in Figure 1. Note that T lymphocytes cannot properly respond to the antigen unless it is processed and embedded in an MHC II molecule. APCs express MHC on their surfaces, and when combined with a foreign antigen, these complexes signal a “non-self” invader. Once the fragment of antigen is embedded in the MHC II molecule, the immune cell can respond. Helper T- cells are one of the main lymphocytes that respond to antigen-presenting cells. Recall that all other nucleated cells of the body expressed MHC I molecules, which signal “healthy” or “normal.”

36. Molecular Basis of Ab Diversity An Antibody or Immunoglobulin is Y Shaped structure consist of 4 polypeptides -2 HC & 2 LC , with 1 Variable region and 1 Constant region. The Structure allows Ab molecules to carry out and dual function,Ag Binding and Biological Activity Mediation. The Imp. Feature of Vertebrate Immune System is ability to respond to an apparent Limitless array of Foreign Ag. Ig Sequence data accululate , virtually every Ab molecule studied was foundto contain a unique Aas sequence in its variable region but only limited no. of invariant sequences in ts Constant region. The Ab Combine sie made up of VL and VH. The Specificiy of any Combining site deermine by Aas sequences. 3 famlies of Ig genes exist in mammals, 1 HC, 1 KAPPA chain and 1 LAMBDA chain. These clusters contan one or ore Constant region genes and no. of variable region gene segments. The Formation of VR of Light and Heavy Chain requires join of 2 or 3 genetic element by a process of Gene rearrangement. Both Germline and Somatic Cell contribute to Ab Include Somatic Cell Mutation.