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Immunology
| Question | Answer |
|---|---|
| Are central to immune function, they drive specific recognition of foreign substances, enabling targeted immune responses. | Antigens |
| Is any molecule that triggers an immune response by binding to antibodies or T-cell receptors. | Antigen |
| are typically large molecules (≥10,000 Da) with complex 3D shapes. | Antigen |
| can also act as antigens when combined | lipids, and nucleic acids |
| Originate outside the body (e.g., bacteria, viruses, pollen, food proteins, toxins). | Exogenous Antigens |
| These are the most common triggers of immune responses. | Exogenous Antigens |
| Produced inside host cells (e.g., viral proteins made during infection, abnormal proteins from cancer cells). | Endogenous Antigens |
| They are displayed on cell surfaces to alert the immune system to internal threats. | Endogenous Antigens |
| Normal host molecules that are mistakenly recognized as foreign, leading to autoimmune diseases (e.g., insulin in type 1 diabetes, nuclear proteins in lupus). | Autoantigens |
| Abnormal molecules on cancer cells (either mutated proteins or overexpressed normal proteins) that can be targeted by the immune system. | Tumor Antigens |
| Antigen Properties | Immunogenicity, Antigenicity, and Foreignness |
| The ability to induce an immune response | Immunogenicity |
| The ability to bind specifically to antibodies or T-cell receptors. | Antigenicity |
| Molecules that are different from the host’s own proteins/carbs are more likely to be immunogenic. | Foreignness |
| Accessible on the antigen’s surface (can be linear sequences of amino acids or 3D conformational shapes) and bind to antibodies. | B-cell Epitopes |
| Typically linear sequences of amino acids that are broken down inside cells and displayed on major histocompatibility complex (MHC) molecules to T cells. | T-cell Epitopes |
| Small, low-molecular-weight molecules (e.g., penicillin, poison ivy oils, some drugs) that cannot induce an immune response on their own (non-immunogenic) but can bind to antibodies (antigenic). | Haptens |
| When haptens attach to larger host proteins called | Carrier molecules |
| the combined structure becomes immunogenic, triggering antibody production against both the hapten and the carrier. | Carrier molecules |
| Substances added to vaccines to enhance the immunogenicity of antigens, especially weak ones. | Adjuvants |
| They work by stimulating innate immune cells to increase antigen presentation and activate lymphocytes, prolonging antigen exposure in the body. | Adjuvants |
| Antibodies also called? | immunoglobulins |
| are Y-shaped glycoproteins produced by plasma cells that bind specifically to antigens. | Antibodies |
| Located at the tips of the Y arms these have unique amino acid sequences that form the antigen-binding site, determining specificity for a particular epitope. | Variable Regions |
| of one heavy and one light chain combine to create a single binding site; each antibody has two identical binding sites. | Variable Regions |
| Form the stem of the Y and the lower part of the arms. | Constant (C) Regions |
| They determine the antibody class and mediate effector functions | Constant (C) Regions |
| Both heavy and light chains are folded into globular domains with distinct functions V domains for antigen binding, and C domains for structural stability and effector activities. | Domains |
| Enzymes like papain split antibodies into two identical Fab fragments and one Fc fragment | Cleavage Sites |
| crystallizable region that mediates effector functions | Fc fragment |
| Immunoglobulin Classes | IgG, IgM, IgA, IgE, and IgD |
| Monomer, most abundant in blood (75-80% of total Ig); crosses the placenta to provide passive immunity to fetuses; activates complement via the classical pathway; opsonizes pathogens for phagocytosis; neutralizes toxins and viruses. | IgG |
| Pentamer (held by a J chain), first antibody produced during an immune response; high avidity (10 binding sites) makes it effective at agglutinating pathogens and activating complement; found in blood and lymph; serves as a B-cell receptor. | IgM |
| Dimer or monomer, primary antibody in mucosal secretions (tears, saliva, breast milk, gastrointestinal fluids); protects mucosal surfaces from pathogens; breast milk IgA provides passive immunity to infants; monomer form is present in blood. | IgA |
| Monomer, lowest concentration in blood; binds to receptors on mast cells and basophils; triggers degranulation (release of histamine and other mediators) during allergic reactions and defense against parasitic worms. | IgE |
| Monomer, mainly found as a B-cell receptor (along with IgM) on naive B cells; function in B-cell activation and maturation is not fully understood, but it may play a role in immune tolerance. | IgD |
| Found in mucous, saliva, tears, and breast milk. Protect against pathogens. | IgA |
| Part of the B cell receptor, activates basophils and mast cells. | IgD |
| Protect against parasitic worms, responsible for allergic reactions. | IgE |
| Secreted by plasma cells in the blood. Able to cross the placenta into the fetus | IgG |
| May be attached to the surface of a B cell or secreted into the blood. Responsible for early stages immunity. | IgM |
| is specific and reversible, driven by non-covalent forces (hydrogen bonds, hydrophobic interactions, ionic bonds, van der Waals forces). | Antigen-antibody binding |
| What are non-covalent forces | Hydrogen bonds, hydrophobic interactions, ionic bonds, van der Waals forces. |
| Antibodies cross-link multiple antigen-bearing particles, clumping them together. | Agglutination |
| This reduces pathogen mobility and enhances phagocytosis | Agglutination |
| Antibodies bind to soluble antigens, forming insoluble antigen-antibody complexes that precipitate out of solution. | Precipitation |
| These complexes are then cleared by phagocytes or the complement system. | Precipitation |
| Antibodies bind to key sites on pathogens or toxins, blocking their ability to attach to host cells. | Neutralization |
| IgG or IgM antibodies bound to antigens activate the classical pathway of the complement system. | Complement Fixation |
| coating pathogens to enhance phagocytosis | opsonization |
| forming membrane attack complexes that destroy bacterial cells | lysis |
| recruiting immune cells to the site of infection | inflammation |
Created by:
Starwitness