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Hypersensitivity Reactions 5 Hypersensitivity reactions IMP Notes Extra Objectives 01 02 03 To know that hypersensitivity To recognize that Type II hypersensitivity deals with To be familiar with inflammatory processes in Type I reactions are over and excessive immune responses against antigens that are integral part of hypersensitivity reaction that mediates allergic immune responses that can be harmful cell membrane and are usually associated with autoimmune inflammation to body in four different disorders ways 04 05 To know that Type III hypersensitivity To describe Type IV hypersensitivity is a purely reactions are mediated by immune complexes cell mediated immune response associated with and cause vasculitis chronic inflammation In other words : over reaction What is hypersensitivity? types of immune reactions desirable reaction undesirable reaction: Hypersensitivity Protective immunity types of hypersensitivity All causes tissue damage IgG or IgM Immediate Delayed Type IV: Type III: Type II: Cell Mediated Type I: IgG antigens IgG or IgM Ab Immunity Immune IgE Ab to tissue antigens Complexes Bind to chemicals or proteins Antibody binding to antigen 01 Type I: Immediate Hypersensitivity Most people will not react to these Non-allergic individuals 01 allergens (antigen causing allergy) but 02 respond to these allergens by some individuals producing IgG antibodies “atopic” respond by producing large Because of the genetic background amounts of IgE in response to those They have two ways to respond to these allergens : of individual that 1-ignore them 03leads to respond in otherwise harmless substances 2-producing IgG Abs abnormal way to allergens Anaphylactic reaction: are severe and rapidly progressing systemic forms which can be quickly life threatening Type I: Immediate Hypersensitivity -allergic (atopic): igE *Occurs within minutes Atopic>have allergy Antibody response to hours and may lead to anaphylactic shock non-allergic ( non-atopic) -non-allergic (non-atopic) : igG *most people > have no allergy Features Cellular components mast cells (involved) basophiles & eosinophils low molecular weight and highly soluble e.g pollens, dust mite, animal Antigens (allergens) dander, nuts, various drugs Injected allergns: hymenoptera (bees, wasps, ants,) sting venom ( a poisonous substance) enters the blood stream causing systemic inflammation & Anaphylactic shock Clinical There is a reaction has similar symptoms of anaphylactic shock called “anaphylactoid reaction” Examples The difference between them :1) non-IgE mediated May result from : (ﻣﺜﻞ اﻷﺷﺨﺎص اﻟﻠﻲ ﺗﻌﺮﺿﻮن ﻟﻸﺷﻌﺔ اﻟﻤﻘﻄﻌﯿﺔ constrast media ( CT (1 2)local anesthetic Diagnosis of -Skin prick test (SPT) putting a small amount of allergens on the skin then prick the skin with a needle and wait for 15-20 minutes to see if there is a reaction allergy - Specific IgE Measurement by testing IgE in the serum -Elimination /Provocation test (Food allergy) avoiding type of food every day until expose the type which cause the allergy ALLERGY IS A SYSTEMATIC DISORDER Reaction Allergic rhinitis Nose Asthma Pharynx Lungs allergy Food Phase I Sensitization phase Esophagus 1 2 Stomach Allergic Anaphylactic reaction reaction First contact with allergen Eczema *Allergic people developed Severe and rapidly progressing urticaria Skin different symptoms allergic dermatitis systemic forms which be quickly life threatening Phase II challenge phase Subsequent contact These reactions will happen in with allergens two phases: Sensitization Primary and secondary mediator First contact with allergen B cell binds to Th2 cell stimulating plasma cell that will produce antibody IgE that binds to a receptor on mast cell surface. *No allergic reaction in Primary *Immediately release this phase Secondary *Not produce until the mast cells/ basophils is activated Challenge Subsequent allergen encounter After being sensitized to the antigen Any future exposure to it will stimulate allergic reaction Type II Hypersensitivity Reactions Hypersensitivity 2 is antibody-dependent process in which specific Antibody IgG (or IgM) antibodies bind to antigens, resulting in tissue damage or destruction Both can activate the complement system -For tissue antigen, not free antigen. -usually associated with autoimmunity Complement Invariable ( constant) activation -Exogenous antigens: Features (microbial) -bound to cell membranes: (Self antigens) Antigens (allergens) In the normal condition, neutrophils attack microbes as antimicrobial action But in type II, neutrophils attack the basement membrane like blood vessels Clinical ●Mismatched blood transfusion (RBCs of Donor will be Attacked by the immune response of The Recipient) ● Glomerulonephritis (anti-glomerular basement membrane) Examples Producing antibodies against glomerular basement > renal failur Diagnosis of Detection of antibodies and antigens by immunofluorescence in tissue biopsy specimens e.g. kidney, skin etc. allergy Type III Hypersensitivity (immune–complex mediated) Antibody IgG or IgM It is activated after formation of immune-complex ( antigen react with antibody) which is capable of inducing an inflammatory response Blood Vessels (vasculitis) Complement Immune-complex Features activation es are deposited in Kidneys (nephritis) tissues like: Joints (arthritis) Type II: was for tissue antigens (cellular antigens). Antigen Free Soluble antigen Type III: for free antigens. ● Glomerulonephritis Clinical Factories made an anti-Immunoglobulin with fluorescent ● Rheumatoid Arthritis dye, they put it on the slide which it may have antigen that examples ● Systemic Lupus Erythematosus (SLE) cause hypersensitivity. If that gene is present, then all the slide will be fluorescent. Diagnosis Immuno-complexes detection in blood/tissue using Immunofluorescence Hypersensitivity III reactions Comparison between immediate hypersensitivity 1-Free antigens binding to 2-Complement antibodies which cause activation Type 1 Type 2 Type 3 3-Recruitment -Antibody: IgE Antigen: Antigen: of inflammatory bound to Antibody: -Antigens:pollens Free soluble Ag cells cell IgG or IgM , dust mite, animal membrane dander, nuts, Ab binds to target various drugs cell them go through Ab bind to target and blood circulating to stay deposit the tissue in the normal state, phagocytes (neutrophils/macrophages) will clear out the immune-complexes after the immune reaction. But in type III reaction, the immune-complexed will be bigger in size so it will be hard for phagocytosis the complexes Type IV Hypersensitivity Known as delayed type hypersensitivity-DTH (2-4 days ; 48h-72h) and cell-mediated hypersensitivity Antibody No antibodies (cell-mediated) Features Cells involved Generally CD4 and occasionally CD8 - CD activates macrophages via Th1 Antigen Presented to T cells by APCs (involving both MHC classes) Pathophysiology of Contact dermatitis: Contact dermatitis Granuloma formation *Not to be mixed with Type I The hapten (eg. nickel which is found in some allergic dermatitis accessories ) : is small molecule that has to bind Skin layers: with protein carrier 1-Stratum (found on the surface of corneum skin) to be activated then 2-Epidermis Clinical *APC in skin make the reaction (Type 3-Dermis IV hypersensitivity) (Langerhans + processed Ag) examples After activated it will will be taken to the close lymph node recruited back to the to have the ability to activated challenge site T helper cell (CD4) , and in some cases CD8 1-Delayed skin test (Mantoux test/Tuberculin test) The Mantoux skin test consists of an intradermal injection of 0.1 ml of PPD tuberculin (Tuberculin Purified Protein Derivative) for 24-72 hours then measure the diameter of the reaction 2- Patch test (used for contact dermatitis) It’s done to see if a particular substance is causing Diagnosis allergic reaction or not. In this test, allergens are applied .then placed on your skin for 48-72 hours(زي اﻟﻠﺼﺎق اﻟﻠﻲ ﻓﻲ اﻟﺼﻮرة) to patches During this time you should avoid bathing or sweating. 3- Lymphocyte transformation test Take Sample of blood on slide, add the antigen and wait to see if, the blood will recognize that antigen or not Reaction Phases Of delayed Mediators released by T-DTH hypersensitivity (type IV): Phase I (1-2 weeks) > Sensitization phase CD4+ Th1 (generally) or CD8+ (occasionally) are activated by APCs like (macrophages *Not to be mixed and langerhans ) with challenge via MHC Class I or II and become T-DTH phase in (delayed type T cell). hypersensitivity I Phase II (24-72 hours) > Effector phase Sensitized T-DTH secretes chemical mediators to (activate macrophages) that act non-specifically Chemical mediators are: More Details about - Chemokine - IFN-후 chemical mediators -TNF ⍺ & β - IL-3/GM-CSF Macrophage activation increases the following: - MHC Class II -TNF receptors -ROS -Nitric Oxide Take home message : Type I (IgE), II (IgG) and III (IgG) hypersensitivity reactions are mediated by antibodies whereas Type IV hypersensitivity reaction is a cell mediated immune response. Hypersensitivity reactions are undesirable, excessive, and aberrant immune responses associated with disorders such as allergy, autoimmunity and chronic inflammation. Quiz Question 1:The cause of allergy A - antibodies B-allergens C- T cells D- all of them Question 2:Antibody type in hypersensitivity II A -IgE B-IgM C-IgG D- IgG & IgM Question 3:how we can diagnose type II hypersensitivity: A - Immunofluorescence B-patch test C-prick test D- RAST Question 4:which one considered as cell mediated hypersensitivity A - Type I hypersensitivity B-Type II hypersensitivity C-type III hypersensitivity D-Type IV hypersensitivity 4-D 3-A 2-D 1-B team leaders Hessah Fahad Alalyan Faisal alotaibi ● Asma Alamri ● Abdulaziz alamri ● Fatimah Almeather ● Abdulaziz alrabiah ● Nourah Almasaad ● Hamad Almousa ● Renad AlOsaimi ● Homoud Algadheb ● Sara Alrashidi ● Mohammed albabtain ● Sarah Alqahtani ● Salih Alqarni ● Shatha Aldhohair ● Osama Mobeirek ● Yara Alzahrani [email protected] editing file click here.
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