Immunity Flashcards
Innate defences (non-specific resistance) - first line
Mechanical barriers - skin, mucous membranes
Chemical barriers - stomach acid, lysozyme
Innate defences (non-specific resistance) - second line
Antimicrobial proteins
Natural killers cells (NK cells)
Phagocytes
Inflammation
Fever
Adaptive defences - immunity or specific resistance
Specific invading pathogens
Specificity - individual agents are different
Memory - second response is greater and faster
Antigens - non-self
Antigen receptors on lymphocytes
Immunocompetence
Recognise specific antigens
Formation of lymphocytes
T cells develop in thymus
B cells develop in red bone marrow
Antigen-activating Immunocompetence lymphocytes - effector and memory cells
B cells (lymphocytes)
Develop in red bone marrow
Once stimulated they clone to become plasma cells which produce antibodies; immunoglobulins (Ig)
Antibody mediated or humoral response
Antibody-antigen actions
Neutralisation - enhances phagocytosis
Agglutination - enhances phagocytosis
Precipitation - enhances phagocytosis
Complement - enhances phagocytosis and inflammation, leads to cell lysis
Antibodies (immunoglobulins) classes
IgG - main antibody and able to cross placenta
IgA - secretory antibody
IgM - released into plasma, indicates current infection
IgE - associated with allergies and parasitic infections
IgD - attached to B cells, antigen receptor
T cells (lymphocytes)
Migrate to thymus to continue development
Cell mediated immune response - intracellular pathogens
T killer cells - directly attack antigen
T helper cells - help both antibody-mediated and cell mediated responses
Memory cells
‘Memory’ of invading antigen
Allows the second and subsequent response to be quicker and much greater
End result - signs and symptoms are not seen
Primary response
Slow and ineffective
Signs and symptoms are seen
Occurs after a delay
Secondary response
Mulch faster and greater
Signs and symptoms not seen
Memory cells
Humeral immunity - active
Natural - infection; contact with the pathogen
Artificially - vaccine; dead or attenuated pathogen
Humeral immunity - passive
Natural - antibodies passed from mother to fetus via placenta or infant in her milk
Artificially - injection of immune serum (gamma globulin)
Autoimmune responses
Fails to recognise the body cells/tissues as self
The immune system attacks its own tissues
Autoimmune diseases - multiple sclerosis (MS)
Destroys the myelin (white matter) of the nervous system
Autoimmune diseases - rheumatoid arthritis
Destroys the cartilage of joints
Autoimmune diseases - type 1 (insulin-dependent) diabetes mellitus
Destroys insulin producing cells of the pancreas
Autoimmune diseases - glomerulonephritis
Destroys the functional units (nephrons) of the kidney
Autoimmune diseases - myasthenia gravis
Impairs communication between nerves and skeletal muscle by destroying receptor sites
Allergy
When a person reacts to a substance normally tolerated by most other people
Antigens = allergens
E.g. pollen, dust mites, diary products, sea food
Allergy - sensitisation stage
Allergen invades
Plasma cells - IgE antibodies which attach to mast cells in body tissues and to circulating basophils
Allergy - subsequent responses
Allergen combines with IgE
Triggers degranulation and release of histamine and other chemicals
Histamines - blood vessels dilate and leaky; promote edema, secretion of mucus, smooth muscle contract
Hypersensitivity reactions - anaphylactic reactions
Breakdown of mast cells and basophils
Result in an anaphylactic shock
Hypersensitivity reactions - cytotoxic reactions
Typical of incompatible blood transfusions
Results in destruction of cells
Hypersensitivity reactions - immune complex reactions
Results in the destruction of tissue
E.g. rheumatoid arthritis, glomerulonephritis
Hypersensitivity reactions - delayed hypersensitivity reactions
Appear 12-72 hours after exposure
E.g. the Mantoux skin test for TB
