Chapter 1 final Flashcards
Four Main tasks of the immune system
Recognition (detection)
Effector Functions (elimination)
Regulation (controlled response)
Memory (protection)
3 forms of recognition
pathogens, self v non-self, danger
Effector functions
Response to recognition via complement, antibodies, cytotoxic cells; Elimination or neutralization of non-self; have exogenous and endogenous targets
exogenous targets
microbes, allergens
endogenous targets
tumors
functions of regulation
avoid autoimmunity, avoid hypersensitivities
functions of imm memory
basis for natural protection and vaccines
is protective immunity immediate or does it take time
takes time. its why new pathogens are so much more deadly
What is greatest achievement in the field of immunology?
vaccines
first vaccine- who and what?
Dr Edward Jenner in the late 18th century was 1st to use a vaccine made up of a related less pathogenic virus (Cow pox) to vaccinate against small pox. Last natural small pox- 1977
Who was Benjamin Waterhouse
promoted vaccines in the US
Who was Andrew Wakefield
said MMR vaccine caused autism
Polio
FDR, iron lungs
3 lessons from vaccines
exposure produces protection, gain specific immunity, large diversity of pathogens
4 Important concepts in Immunology
memory
specificity
diversity
self v nonself
Pathogens
Micro-organisms (infectious organisms) that cause disease. They can be known infectious agents or ones that normally colonize the body.
microbiota
The community of micro-organisms that our bodies contain / commensal species of micro-organisms, which live primarily in the gut and on the skin.
Commensal micororganisms
Most commensal species are benign or beneficial. We have co-evolved to take advantage of beneficial relationships. They aid in human nutrition by helping with digestion and making vitamins. They also block colonization by pathogenic organisms
Effect of antibiotics on commensal bacteria
antibiotics can kill commensal bacteria in the gut and allow for pathogenic bacteria to take over.
4 classes of pathogens
bacteria, viruses, fungi, and parasites
Emerging pathogens have higher mortality rates because…
- they have not adapted to their host yet- pathogens dont want to kill their hose
- the host has no adapted to them yet, they have no defense against the pathogen
Opportunistic pathogens
Microorganisms that normally do not cause disease. They cause illness (disease) if body’s defenses are weakened (immunocompromised person) or if they get into ”wrong” place (immunologically privileged sites, or gut pathogens leaking into the blood)
3 levels of defense against infection
1) barrier function- skin and mucosal surfaces
2) innate imm response
3) adaptive imm response
Epithelium
impenetrable barrier (physical)
Mucosal surfaces (mucosae)
epithelial lining (continuous with skin) of respiratory, gastrointestinal and urogenital tracts; Continually bathed in mucus that they secrete; Mucus is a thick substance made up of glycoproteins, proteoglycans and enzymes
All epithelial surfaces secrete…
antimicrobial substances (peptides, enzymes etc.,); Tears and saliva contain the enzyme lysozyme which dissolves the cell wall of bacteria
3 types of defenses barriers have
mechanical- flow of fluid, cells joined by tight junctions
chemical- defensins, enzymes, etc
microbiological- normal flora
innate vs adaptive imm
innate
- Physical and chemical barriers; White blood cells such as phagocytic macrophages, neutrophils; Rapid response minutes, hours; Ancient system plants, animals
adaptive
-Lymphocytes with specialized receptors; Specificity and diversity; Requires days to develop; Memory
Inflammation is caused by the ___ imm response
innate
2 phases of innate immune resonse
1) recognition- via PAMPs and then marked nonspecifically with complements
2) recruitment of effector cells that destroy the pathogen
Complement
a system of plasma proteins that can be activated directly by pathogens or indirectly by pathogen-bound antibody, leading to a cascade of reactions that occurs on the surface of pathogens and generates active components with various effector functions
stages of complements
1) bacterial cell surface induces cleavage and activation of complement
2) one complement fragment covalently bonds to the bacterial, the other attracts an effector cells
3) The complement receptor on the effector cell binds to the complement fragment on the bacterium
4) the effector cell engulfs the bacterium, kills it and breaks it down
5 hallmarks of inflammation
heat, redness, swelling, pain, and loss of function
2 major inflammatory cells
neutrophils (blood) and macrophages (tissue)
clonal selection
start out with many lymphocytes with different specificity-> Only those lymphocytes that recognize the pathogen expand and differentiate into effector cells
