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innate defenses
have no memory, non-specific
self-antigens
molecules considered “self” in which immune cells should ignore
auto-immune response
immune cells are activated by self-antigens
foreign antigens
immunogens, activate the immune system
Pathogen-associate molecular patterns (PAMPS)
molecular structures on pathogen surfaces
pattern recognition receptors
how immune cells recognize PAMPS
pathogen
infectious and cause disease
criteria to be a pathogen
arrive at the body surface of a host, enter the host’s body or enter a portion of the host’s body, evade defenses, multiple inside host, infect a new host
there is communication between
immune cells, normal cells and infected cells
types of innate defenses
barriers, fever, chemicals, phagocytes, natural killer cells and inflammation
types of first line of defense
skin, mucous membranes, secretions of skin and membranes, normal flora
types of second lines of defense
phagocytic cells, complement system, antimicrobial proteins, inflammation, fever
what happens in a fever
viral or bacterial infection stimulates some immune cells to proliferate and secrete proteins which raise the thermoregulatory “set point”
purpose of fever
elevated body temperature inhibits microbial growth by causing the liver and spleen to take up iron, making it not available for bacteria for their metabolism and it also increases phagocytic activity
interferons
proteins released by virus-infected cells to their neighbors
purpose of interferons
help protect cells that have not been infected, they cause cells to interfere with viral replication
complement
a group of proteins that function in innate immunity, (activation, protein cascade, response), all complement activate leads to activated C3b
classical pathway
complement proteins bind to antibody bound to antigen
lectin pathway
lectin proteins bind carbohydrates on microve surface
alternative pathway
complement protein C3 spontaneously cleaves to C3a and C3b
membrane attack complex (MAC)
protein complex from complement that attaches to membrane of the bacteria and makes holes in it (leads to lysis)
enhanced inflammation from complement
complement proteins bind to basophils and they release inflammatory mediators
neutralized viruses
C3b proteins from complement can surround a virus and neutralize their functions
opsonization
bacteria is coated by C3b proteins and can be more easily phagtocytized by macrophages
how leukocytes are involved in defenses
innate immune system cells are attracted and activated by chemical signals on the surface of pathogens
Natural killer cells
recognize infected cells and cancerous cells and induce these cells to undergo apoptosis, they are in blood and lymph
inflammation
helps maintain homeostasis
first steps of an inflammatory response
PAMPs or internal cell stress signals bind to PRRs on leukocytes, which they release inflammatory signals
systemic responses from inflammatory mediators
change in endothelial permeability, vasodilation, facilitate immune cells leaving the blood stream, recruit other immune cells to site
mast cells
immune cells that detect foreign substances in the tissue spaces and initiate local inflammatory responses against them
histamine
release by mast cells to promote vasodilation of local arterioles and permeability of capillaries
cytokines
inflammatory mediators released by macrophages
exudate
leaks from capillaries, contains fluid, clotting factors and antibodies and other proteins like complement, late swept into lymph vessels
Phagocyte mobilization steps
margination, diapedesis/extravasation, chemotaxis
margination
phagocytes enter blood from bone marrow and cling to capillary wall due to adhesion molecules in endothelial
diapedesis/extravasation
phagocytes flatten and squeeze out of capillaries
chemotaxsis
cells follow the chemical trail to injury/infection site