Innate/Adaptive Immunity Flashcards
immune response
body’s ability to defend against specific pathogens/foreign substances that develop decease-initiated by the body’s defense systems
innate immunity
-born with (inborn
-first line of defense
-ready state-before infections appear
-not antigen-specific
-early, rapid response
-directs/controls adaptive responses
adaptive/acquired immunity
-acquired
-second line of defense
-antigen-specific (foreign pathogens)
-retains “memory” of pathogens
-later response (days later)
-involves membrane
-distinguishes self vs non self
cytokines
-proteins secreted by cells (macrophages) of the innate and adaptive immunity (Its, IFNs, TNF-a)
-“cell signaling”
chemokines
cytokines that stimulate migration and activation of immune and inflammatory cells
colony-stimulating factors (CSF)
stimulate growth and differentiation of bone marrow progenitors of immune cells
granulocyte CSFs (G-CSF)
CSFs that the promote growth and maturing of neutrophils consumed in inflammatory reactions
innate immunity characteristics
-physical barriers (epithelial cells, mucous membranes)
-monocytes/macrophages
-neutrophils (early arrivers
-natural killer cells
-complement system-cells/molecular components in the inflammatory process
epithelium in innate immunity
-has a high turnover rate-frequently washed (GI system, urinating, sneezing, coughing)
-physical barrier, blocks entry of infectious agents (ex: microbes)
-secretes antimicrobial enzymes/proteins/peptides
mechanisms of innate immunity
-monocytes/macrophages engulf and digest microbes-then remember what they ate and signal other parts of immune system
-neutrophils engulf and digest microbes-act as a signal for the site
-NK cells kill microbes and foreign agents (but don’t respond to specific antigens)
leukocytes in innate immunity
-move to infected areas, engulfs bacteria through phagocytosis
-then lysosomes digest the bacteria and breaks it into small proteins
natural killer cell receptors
-NK cells have activating receptors that respond to: ligands from virus-infected or injured cells, and inhibiting receptors binding to MCH-1 self-recognition molecules (from normal cells)
why aren’t normal cells killed in the immune response?
-inhibitory signals from normal MHC-1 molecules override activating signals (in virus/tumor-infected cells the inhibitory receptor is not engaged, which allows activating for cell killing)
compliment system
-system inside of the blood that is essential for the activity of antibodies
-activation increase bacterial clumping which makes them more prone to phagocytosis (“tagging”)
-has 3 phases: initial activation phase, early-step inflammatory responses, late-step membrane attack response
recognition systems
-pathogen-associated molecular patterns (PAMPs) are recognized by pattern recognition receptors (PRRs) like toll-like receptors (TLRs)
innate immune recognition
-not as specific
-receptors have limited diversity
-molecular patterns that are common to microbes
-effector cell types have identical receptors
-self-nonself discrimination by recognizing molecules of pathogens (NKs recognize MHC-1 molecules)
adaptive immune recognition
-specific microbial molecules and distinct antibodies
-large diversity expressed through somatic genes
-clones of lymphocytes have unique receptors
-self-nonself discrimination by lymphocytes using MHC-1 and foreign peptides for recognition