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Microbio L13
| Question | Answer |
|---|---|
| Immunodeficiency | lack of proper immune response Could have a partial/weak response, or no response Difficulties fighting off infections |
| Primary immunodeficiency | genetic, born with it Rare, but more severe Affected pathways: 50% B cells, 30% T cells, 18% phagocytes, 2% complements |
| SPUR | Severe infections Persistent infections Uncommon infections Recurrent infections |
| Secondary immunodeficiency | acquired, get it later in life Much more common Caused by: Aging Some disorders (diabetes, malnutrition) Some drugs are immunosuppressive Some infections |
| Immunodeficiency may lead to | cancer |
| Autoimmune disorders | Immune system attacks the body Loss of tolerance Systemic vs localized Diagnosed via autoantibodies Treated with immunosuppressants |
| Hypersensitivity | An inappropriate adaptive immune response Could be to self antigen (autoimmune) Could be harmless non-self antigen |
| Hygiene hypothesis | cleanliness lowers microbiome diversity, decreases training of immune system, can lead to hypersensitivity Just like what you learned in anatomy |
| Hypersensitivity usually cannot be | Usually cannot be cured, just treated Immunosuppressants 4 types, differentiated by active immune pathway, and triggering antigen |
| The 4 types of hypersensitivity: | 1. Allergies 2. Cytotoxic 3. Immune Complex 4. Delayed Hypersensitivity |
| Type 1 | Allergy!!! Triggered by harmless antigens called allergens All allergies, along with some asthma and some skin eczema Activation of IgE and mast cells!!!!!! |
| Route of exposure to allergen determines | symptoms |
| A reaction is called | Anaphylaxis!! Can be localized or systemic |
| Exposures to type 1 hypersensitivity Primary exposure | first time, B cells make IgE Sensitization |
| Exposures to type 1 hypersensitivity Secondary exposure | subsequent times, IgE on mast cells causes degranulation, symptoms Histamine is big driver!!! |
| Treatment for type 1 hypersensitivity | Avoid allergen Manage symptoms Anti-inflammatory drugs Epinephrine and respiratory/systemic anaphylaxis |
| Sensitization | repeated exposure converts Th2 into Th1 cells, less IgE |
| Type 2 hypersensitivity | Cytotoxic (usually) Activation of IgG and IgM Binds to non-soluble agent |
| Cytotoxic Type 2 hypersensitivity | Antibodies bind to target, and induce killing via other immune pathways - Cytotoxic Either Recruit complement proteins to kill Recruit NK (innate) cells to kill) |
| Non-Cytotoxic Type 2 hypersensitivity | Antibodies bind targets and block some crucial signaling pathways |
| Type 3 hypersensitivity | Immune complex Activation of IgG and IgM Binds to soluble antigen Antibodies and antigen form large complex Deposits in tissues Recruits complement to cause damage |
| Many of these type 3 hypersensitivities are | autoimmune Some not Example: antibody treatments and serum sickness |
| Type 4 Hypersensitivity | Delayed hypersensitivity 12-72 hours after contact Activation of T cells Slow activation, hence “delayed” |
| More on Type 4 Hypersensitivity | Reacting to self or non-self antigen Requires a sensitization step for T cells to activate Must be exposed to triggering antigen at least once to occur |
| Autoimmune Type 4 hypersensitivity | T cells attack some antigen |
| Non-autoimmune type 4 hypersensitivity (most common) | Attack induced by non- self antigen • Usually a tiny hapten that merges with a self- protein Ex. • Contact dermatitis (poison ivy, latex allergies, nickel/metal reactions) • Tuberculosis PPD test |
Created by:
liladdoyle