Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
immuno final K338
hyperactivity, tolerance, transpalntation, vaccines
| Question | Answer |
|---|---|
| Immediate Hypersensitivity includes: | Type I- mediated by IgE Type II- mediated by IgG and IgM Type III- mediated by immune complexes |
| Delayed Hypersensitivity DTH- Delayed Type Hypersensitivity | Type IV- cell mediated DTH- is the second major form of cell mediated immunity,and is controlled by helper T cells. A DTH response is basically an inflammatory response induced by T helper cells. DTH effector cell is non antigen specific--the macrophag |
| T Helper cells control: | DTH- Delayed Type Hypersensitivity Humoral immunity and cytotoxic T cell responses. |
| DTH responses | DTH responses occur to specific types of antigen like intracellular bacteria and certain chemicals.BUT THE DTH EFFECTOR CELL IS NON ANTIGEN SPECIFIC--MACROPHAGE |
| Intracellular bacterial which induces Type IV Hypersensitivity | Mycobacterium tuberculosis |
| Virus which induces Type IV Hypersensitivity | Herpes simplex Variola (Smallpox) Measles |
| Contact antigens which induce Type IV Hypersensitivity | Poison Ivy Poison Oak Candida Albicans- yeast infections |
| The 2 Phases of DTH Response | 1. Sensitization Phase-activates T cells but produces no immediate DTH response 2. Effector Phase- T cells specific for the antigen secrete Cytokines (INF- gamma) that recruit and activate other inflammatory cells, which then mediate the DTH response |
| During the DTH effector phase, TH1 secrete........? | Cytokines INF-gamma, IL2, IL3, TNF-beta, GM-CSF, MIF Chemokines IL8/CXCL8, MCP-1/CCL2 |
| What are the effects of macrophage activation? | Increase in: Class II MHC molecules TNF receptors Oxygen Radicals Nitric oxide |
| What do chemokines do? | Mediate recruitment of macrophages to the site of the antigen. |
| INF-gamma | increases class II MHC expression on macrophages and other cells Activates macrophages and causes them to release additional inflammatory mediators |
| TNF-Beta | Mediates macrophage activation, local tissue destruction, and alters adhesion molecules on local blood vessels endothelium to faciclitate extravasation of other cells like neutrophils |
| IL-3 and GM-CSF | enhances monocyte production by bone marrow |
| The macrophages which are recruited by T cells during DTH effector mechanism can..... | undergo respiratory burst and produce oxygen radicals which kill bacteria produce nitric acid phagocytose cellular debris secrete cytokines esp TNF-alpha continue to present antigen and stimulate helper T therefore continuing the rxn until antigen is |
| DTH rxns generally cause | localized tissue swelling 24 to 72 hours after initiated |
| How are DTH reactions measured? | They are measured by skin texts. The antigen is injected intradermally and if a DTH reaction occurs swelling and inflammation will appear at the site 2-3 days later. |
| When does chronic inflammation occur? | When the bacteria cannot be destroyed or phagocytosed or when the antigen is self antigen. |
| Chronic inflammation sites are marked by ? | Accumulation of macrophages and formation of fibroid scar tissue. Fibrose scar tissue can become granulomas. |
| Granulomas | a central area of fibrotic tissue and activated macrophages ( many of which fuse and become multinucleated giant cells) surrounded by lymphocytes. |
| What makes an antigen an allergen? | ability to induce a TH2 driven response recipients genetics relevant enzymatic activity |
| What cells are involved in Type I Hypersensitivity allergic reactions? | Mast cells and Basophils. Mast Cells and Baasophils posses receptors for the Fc region of IgE (Fc&RI) |
| Common allergens associated with Type I Hypersensitivity | Proteins- from foreign serum and vaccines food plant pollen drugs mold Species insect products |
| ?? How does degranulation happen? | look up |
| What are the vasoactive mediators released during degranulation? | histamine, leukotrienes, prostaglandins, cytokins |
| What is the treatment for systemic allaergic reactions? | Epinepherine which counteracts the effects of allergic mediators on smooth muscle and vasculature. |
| Allergen Immunothereapy | the practice of administrating gradually increasing quantities of of an allergen extract to an allergic subject to ameliorate the symptoms associated w subsequent exposure to the causative allergen |
| Mechanism of Immunotherapy include: | Modifying T cell responses by either immune deviation [shift from TH2 to TH1]. T cell anergy, or most likely both. RISK SYSTEMIC ANAPHYLAXIS REMENBER IgG should go up and IgE should go down |
| Type II Hypersensitivity | Innapropiate antibody mediated destruction of cells via complement, ADCC, and opsonization. occurs in any circumstance where cells are exposed to high levels of cell reactive antibody. EX; transfusion, and Rh syndrome |
| When there is a blood transfusion reaction the terminal sugar residue on red cell glycoproteins cross reacts with ,,,,? | antigen present on intestinal microorganisms. |
| What type of Hypersensitivity is Drug-induced hemolytic anemia? | is a type II hypersentitivity, bc its antibody mediated destruction of cells via complement. |
| Drug-induced hemolytic anemia | Some drugs bind to erythrocyte proteins and create novel epitopes. Some individuals make an IgG response to these epitopes. The resulting IgG antibodymay mediate complement lysis of red cells leading to hemolytic anemia. |
| Typical manifestations of type I Hypersensitivity | Systemic anaphylaxis and local anaphylaxis such as hay fever , asthma, hives, food allergies, and eczema. |
| Typical manifestations of type II Hypersensitivity | Blood transfusion reactions Erythroblastosis fetalis autoimmune hemolytic anemia |
| Typical manifestations of type III Hypersensitivity | localized Arthus Reaction and generalized reactions such as serum sickness, necrotizing vasculitis, glomerulonephritis, rheumatoid arthritis, and systemic lupus erythematosus. |
| Typical manifestations of type IV Hypersensitivity | contact dermatitis, tubercular lesions, graft rejections |
| How are immune complexes created? | Binding of antibody to soluble antigen creates immune complexes, |
| Type III Immune complex mediated Hypersensitivity | AG-AB complexes deposited in various tissues induce complement activation and insuring inflammatory response mediated by massive infiltration of neutrophils. |
| Example of serum sickness | injection of horse antitoxins into an individual previously sensitized to horse immunoglobulin |
| Symptoms of serum sickness include....... | including fever, rashes and sometimes glomerulonephritis as a result of immune complex deposition in the kidneys. |
| The three major types of graft rejection in solid tissue transplantation are | Hyperacute, Acute, Chronic |
| Vaccination | Any immune manipulation that provides protection from disease |
| Passive immunity | immunization that provides protection against a specific pathogen but does not require the recipient to make an immune response. Transfer of antibodies or cells |
| Advantages of recombinant vector vaccines | Cheap to manufacture and administrate, Stable do not require refrigeration, Stimulate both humeral and cellular immunity, Poxvirues have a large genome and could express a large number of foreign antigen |
| Primary Immune Deficiency | genetically determined |
| Secondary immune deficiency disorder | arising from a non genetic cause ex infection |
| BLS Type I | Deficiency of MHC Class I expression, Decreased number of CD8+ T cells, Variable susceptibility to viral infections, Normal Humeral immunity and DTH, Abnormal CTL responses, Caused by beta2 microgobulins abnormalities or defects in TAP gene |
| XLA | Genetic defect that prevents maturation of B cells past the pre/pro B cell stage |
Created by:
dr. ada
Popular Biology sets