Unit II Flashcards
Infection
definition
presence and multiplication of pathogens
Pathogen
definition
disease causing agent
what primarily defends the body from infection
spleen and lymph nodes
mechanisms of defense
innate (nonspecific) defense
adaptive (specific) defense
Innate (nonspecific) defense
“inborn” protection against many types of pathogens
^^don’t develop as a result
Adaptive (specific) defense
2 forms of immunity?
“learned” protection against specific pathogens provided by T and B cells
-cell mediated immunity
-antibody mediated immunity
Cell-mediated immunity
T cell function
cells attack pathogens and attack through phagocytosis or release of chemical toxins
Antibody-mediated immunity
B cell function
secrete antibodies, work indirectly, attack by circulating antibodies
Innate (nonspecific) defenses
what kinds of natural things help defend?
physical barriers such as skin, mucus membranes
phagocytes
immune surveillance such as natural killer cells (lymphocytes) = find abnormal cells and cause destruction
interferons (chemicals released to protect you)
complement system
inflammation
fever (low grade fever beneficial for combatting infection)
Natural Killer cell process
-NK cell releases perforins, which stick to each other and form a hole in enemy cell membrane
-granzymes from NK cell enter perforin hole and degrade enemy cell enzymes
-enemy cell dies
-macrophage engulfs and digests dying cell
Inflammation
signs and reasons why
goal of inflammation
would causes come from?
-Redness and heat (due to increased blood flow to site)
-swelling (due to increased capillary permeability)
-Pain (due to tissue fluid pressure and inflammatory chemicals stimulating pain receptors)
-goal: get WBC to area to fight bad cells
-come from blood, mast cells, WBC, damaged tissues
Complement system
what is it
end result
what does it promote
-involves large number of plasma proteins
-end result: formation of a membrane attack complex that forms holes in pathogen cell membranes
-promotes phagocytosis, inflammation, chemotaxis
Inflammation Chart Diagram
Tissue damage occurs –> bacteria enters tissue –> chemical mediators are released (WBC, damaged cells) –> chemotaxis, increased vascular permeability (capillaries leaky), increased blood flow –> increased numbers of white blood cells and chemical mediators at site –> bacteria are contained, destroyed, and phagocytized –> either bacteria gone = tissue repair OR bacteria remain = additional chemical mediators activated
Adaptive (Specific) Immunity
terms
Adaptive immunity
antigen
activation
proliferation
differentiation
Adaptive immunity
resistance to a specific pathogen
Antigen
-any molecule capable of binding to a T cell or B receptor
-usually part of a pathogen (ex. bacterial or viral protein)
Activation
change in behavior of lymphocyte at the onset of immune response
Proliferation
production of a large number of identical lymphocytes (Clone)
Differentiation
production of cells with different functions from a single line
T Cell characteristics
-produced in red bone marrow
-mature in thymus
70-80% of circulating lymphocytes - most common
-many reside in lymph nodes and spleen
-millions of different T cell receptors that bind to antigens
-another cell has to show to T cell
Antigen Presenting Cell info
-typically a macrophage, B cell, or infected cell
-the antigen is presented to T cell in combination with a major histocompatibility complex
-antigen “selects” the T cell that will be activated and proliferate to form a clone (clonal selection)
Major histocompatibility complex
what are the classes?
Class I - on nucleated body cells and platelets
Class II - on antigen presenting cells
Main Types of T cells
helper t cells
cytotoxic t cells
memory t cells
Helper T cells info
Activation requires APC
secrete cytokines that target other WBCs
activate B cells to produce antibodies
activate cytotoxic t cells
Stimulate macrophages and attract other WBC