Qi Micro Immunology Lecture Notes PDF

At the end of this lecture, the students should be able to: I...

At the end of this lecture, the students should be able to: I  Understand types of immune system disorders  Identify the hypersensitivity and allergy  List the different types of hypersensitivity reactions  Explain the mechanisms of different types of hypersensitivity & State examples on each type  Recognize the different clinical manifestations of hypersensitivity and autoimmunity  Mention different methods of treatments and prevention ‫اللهم ال سهل إال ما جعلته سهال‬  Understand immunodeficiency causes & management ‫اللهم علمنا ماينفعنا وانفعنا بما علمتنا وزدنا علما‬ Type I (immediate) hypersensitivity (Allergy ) Hypersensitivity Reactions am 4 types of Hypersensitivity (Exaggerated immune response) overreaction of the immune system against foreign harmless / environmental substances (allergen) by production of IgE antibodies - Types I, II, III are antibody mediated Type I, : anaphylactic reactions.  The allergen(Antigens that induces production of specific IgE )may enter the body through: Type II: cytotoxic reactions. Type III,: immune – complex Type I (immediate) hypersensitivity (Allergy ) inhalation (pollens, house dust,…) ingestion (fish, egg, strawberry,…) contact (wool, nylon, cosmetics,...) time - Type IV is cell mediated injection ( IV antibiotics e.g. Penicillin, insect bites,…) Type IV, Delayed hypersensitivity In some people, the immune system recognizes certain substances e.g., drug or food as foreign or dangerous…. The response ranges from localized allergic reaction to systemic anaphylaxis/shock OR death mm As a result, the immune system reacts by making a type of antibody called Trigger: - harmless environmental substance immunoglobulin E (IgE) to defend against the allergen. This reaction leads to - infection allergy symptoms - self-antigen The reaction starts immediately 15 99 swim 45 4 16  Antigen stimulates formation of antibody (Ig E type)  Histamine:  Immediate phase: Within minutes  IgE fixes, by its Fc portion to mast cells  Dilates and increases permeability of blood In  Ready performed mediators (histamine) vessels (swelling and redness),  Re-exposure to the same antigen (allergen)cross-link between Ig E  increases mucus secretion (runny nose), antibodies(fixed to mast cells) leading to activation and degranulation  smooth muscle contraction (bronchi). of mast cells and release of mediators (immediate phase) name  Slow-reacting substance of anaphylaxix (SRS-A) :  Late phase: 6 hours after exposure  several leukotrienes. slow onset of effect mediators e.g. Leukotrienes a  degranation  Air ways constriction(bronchospasm) Asthma lean  slow onset of effect. Type I (immediate) hypersensitivity (Allergy ) Local anaphylaxis urticaria Allergy is Ig E mediated rubber latex allergy and dental (type I: immediate practice hypersensitivity Allergic eczema Penicillin Allergy       Avoidance of the allergens (Prevention) Good History taking , antibiotic sensitivity test before injection Emergency life saving>> Maintenance of an airway Support of respiratory and cardiac function Drugs to counteract the action of mediators Epinephrine?, antihistaminic?, corticosteroids If Type II (Cytotoxic/cytolytic) hypersensitivity    Cytotoxic hypersensitivity occurs when antibody IgG or IgM is directed against self-antigens of the cell membrane region. It activates via its Fc region: (autoimmunity) antibody (IgG or IgM) attaches to the target cell membrane via its Fab Complement: generates a membrane attack complex, which damages the cell membrane Attracts phagocytes: opsonization.  Cromolyn sodium  Bronchodilators?  Monoclonal anti-IgE antibody (omalizumab, …) Rheumatic fever: Example of type II hypersensitivity Antibodies produced against untreated bacterial infection namely: Streptococcus pyogenes. The Streptococcal bacterial cell wall antigen cross-reacts/similarity with self-antigen present in blood group incompatibility : antibodies in the recipient's plasma attack antigens on the donor's RBCs. This cause hemolysis the cell of heart  antibodies attack heart  cardiac tissue damage (heart valves) iii Management: iiiiii deservation  fffP 19111196 Immune response if strep. Throat untreated Type III hypersensitivity reactions (immune complex) immunecomplex deposits locally circulation Type III hypersensitivity reactions Clinical types: (immune complex) A- Systemic immune complex disease Autoimmune disease: SLE Systemic Lupus Erythematosus: autoantibodies against DNA (hidden antigen exposed to immune system after cell lysis) Certain infections: e.g., Hepatitis B Virus, HIV allusions in Post Streptococcal glomerulonephritis (streptococci-antibody complex is largely deposited in kidney (common cause of renal failure) Unusual / large amounts of antigen - Antibody complex B- Local Immune Complex Diseases: Arthus reaction: is a local immune complex reaction. Repeatedly injected subcutaneous with antigen, e.g. rabies vaccination. Characterized by erythema, edema and necrosis at injection site inmmeamneantigntanis esfreea r.id Type IV (Cell mediated / Delayed) hypersensitivity Type I, Immediate Mediated by IgE, mast cells and bnasophils Type IV hypersensitivity T.eu Sensitized T helper lymphocytes release lymphokines against antigen and induce inflammatory reaction (attract macrophages, inflammatory mediator). This cellular infiltration induce tissue damage. Also, activate cytotoxic T cells causing direct cellular damage (Delayed, Type II, cytotoxic cell – mediated reactions) Examples: Mediated by IgG or IgM. Occurs on cells. Insulin dependant (type I) Diabetes Vasculitis Type III, immune-complex Mediated by IgG or IgM, soulbe complexes Persistent microbes: Tuberculosis deposition. The tuberculin test reaction is positive if T-cells endothelial injury , facilitating formation of Type IV, delayed type Have been activated by TB infection Types micro thrombi t.ETnoimmanogi.br Mediated by cell mediated immunity. Also activated platelets release vasoactive amines , and help formation of micro thrombi. Graft (transplant) rejection type-I type-II type-III type-IV characteristics (anaphylactic) (cytotoxic) (immune complex) (delayed type) antibody IgE IgG, IgM IgG, IgM None Tolerance prevents immune system responding to self-antigens antigen exogenous cell surface soluble tissues & organs T- cells are initially tolerant of autoantigens in the thymus Central tolerance. response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours Breakdown of T-cell tolerance: appearance weal & flare lysis and necrosis erythema and edema, necrosis erythema and induration Centrally: following inheritance of two different types of genetic poly morphism histology basophils and eosinophil antibody and complement complement and neutrophils monocytes and lymphocytes attacks Peripherally: - hidden antigen exposed to immune system (eg. DNA after cell lysis) transferred with antibody antibody antibody T-cells - Molecular mimicry (eg. rheumatic fever) tuberculin test, poison ivy, erythroblastosis SLE, farmer's lung disease examples allergic asthma, hay fever granuloma fetalis, Goodpasture's nephritis  Oral manifestations of some Autoimmune diseases Genes , infections , Environmental factors Oral signs are frequently the first manifestation of autoimmune diseases. Normal Autoimmune Dentists play an important role in the detection of emerging autoimmune pathologies. autoimmunity disease Early diagnosis play a decisive role in improving the quality of treatment strategies as well as quality of life Examples of Autoimmune diseases which have Oral manifestations systemic lupus erythematosus, Sjögren syndrome, pemphigus vulgaris, mucous membrane pemphigoid, Behcet disease oral manifestations of SLE systemic lupus erythematosus may include: Pemphigus vulgaris systemic lupus erythematosus, oral ulcers, hyposalivation, pigmentations a rare autoimmune disease characterised by painful blisters and erosions on the skin Sjögren's Syndrome and mucous membranes, honeycomb plaques (silvery white, scarred plaques); raised keratotic plaques painful, diffuse oral ulceration autoantibodies against DNA (hidden antigen exposed to immune system after cell lysis) (verrucous lupus erythematosus); and nonspecific erythema, purpura, petechiae, The immune complex deposits in different organs (joints, skin, muscles, eyes, lungs, central autoimmune disease with the biggest impact on oral health is Sjögren's are the initial manifestation in 50 to 80 percent of patients and cheilitis Syndrome. This disease attacks the lacrimal and salivary glands, leading to nervous system, and kidneys), inflammatory reaction, organ impairment confused with other disorders that present lesions like candidiasis, So, Microscopic oral manifestations with SLE were extreme dry mouth(xerostomia) and dry eyes examination highlights epithelial damage Destruction of the exocrine glands because of increased activation of 40% of patients suffer petechial lesion and gingival bleeding due to desquamative gingivitis, B.cells followed by immune complex formation and autoantibody marginal gingivitis, or erosive mucosal lesions due to serious thrombocytopenia. production Diagnosis: Many SLE patients may present at the same time Sjögren syndrome antibodies are detected in the patient's serum Signs and symptoms: Often associated with other autoimmune Lack of saliva predisposes patients to develop tooth cavities. Syndrome such as rheumatoid arthritis. The lack of saliva facilitates the accumulation of plaque and their clearance. Edema and inflammations of the gingiva. , a salivary flow decrease can develop opportunistic infections e.g., Candida is often detected because the lack of lysozyme and immunoglobulins Discrete red and white plaque on the hard palate in a Keratotic, rough-surfaced plaque (verrucous lupus difficulties to speech and metallic sensation in the mouth are characteristic patient with discoid lupus erythematosus. erythematosus) erythema on the palatal mucosa of xerostomia, as well as burning sensation of the oral mucosae pemphigus vk.ittilog comeswitnsorgen i i.EE iiii i.i esiivasnardspean.in Rematoid nm i blague Behcet Disease autoimmune, multisystemic disease of unknown etiology oral ulcers, genital ulcers, and eye inflammation. aphthae of the oral mucosa: lips, buccal mucosa, soft palate, and tongue painful and characterized by Cyclic presentation another clinical explanation is excluded e