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Immunology Flashcards

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Biology 101 flashcards
1
Q

Reason for various immune responses

A

protective to be infected with another worm

nutrition

treatment

immune response

anatomical location of infection

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2
Q

Parts of the Innate branch

A

physical barriers

chemical barriers

microbial barriers - commensals

cellular components - phagocytes and lymphatics

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3
Q

commensal

A

typically does not cause disease

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4
Q

pathogen

A

primary - disease causing

opportunistic - typically commensal but will cause disease in a weakened host

  • also cause disease when relocated to a site that it is not usually found
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5
Q

infection

A

microbe gains access to a host

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6
Q

disease

A

microbe causes symptoms

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7
Q

pathology

A

damage that a microbe directly causes to the host

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8
Q

immunopathology

A

unwanted side effect of immune system

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9
Q

parasite

A
  • organism that feeds off of another organism that provides a host and is damaged in the process
  • ectoparasite - live on the outside
  • endoparasite - lives inside
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10
Q

Latent

A

not replication active and not detectable by culture

-example is EBV and some viruses

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11
Q

Contact infection

A

vector transmitted - typically transmitted via a bite

fomites - inanimate object that can transmit pathogens

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12
Q

Job of the immune system

A

protect you from foreign intruders

distinguish and protect against foreign organisms

detect and protext against foreign organisms

distinguish between self and nonself

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13
Q

About the Innate system

A
  • born with it - innate receptors and germline encoded
  • nonspecific response and receptors
    • Pattern Recognition Receptors recognize PAMPs
  • first line of defense
  • reacts almost immediately
  • NO memory - same response (speed, strength) everytime
  • Components
    • physical
    • chemical - lysozyme
    • microbial - commensals
    • phagocytes engulf pathogens
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14
Q

PAMPs

A

Pathogen Associated Molecular Pattern

-recognized by PRR pattern recognizing receptors

  • Gram + have LTA and PGN
  • Gram - have LPS
  • Fungi - zymosan
  • Viruses - dsRNA
  • helminth - CHO

PAMPs should never be expressed on host cells

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15
Q

About the Adaptive arm

A
  • must be activated by innate signals
  • 5 - 10 day response time
  • has memory
    • second response is faster and stronger
  • very specific receptors that can be tailored
    • recognize antigens
  • Cellular Component
    • T cells - Helper and Killer
  • Humoral Component
    • antibody producing B cells
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16
Q

Physical and Chemical Barriers

A
  • defensins (on the skin, imbed into membrane - lysis), lysozyme (in the tears to degrade PGN), AMPs (antimicrobial peptides), low pH
  • goblet cells - produce mucus. Important in the lungs
  • cilia - wavy motion moves foreign bodies that are trapped in the mucus
  • tight junctions - no gap between epithelial cells
  • vili - intestines, valleys are crypts with high defensin conc.
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17
Q

Cryptosporidium parvum

A

pathogen that evades destruction by stomach acid

parasite eggs are activated by stomach acid

helps time release of parasite into the intestine

-protozoan parasite

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18
Q

microbial barriers

A
  • nutrition competition
  • take up space
  • disrupting commensals can cause opportunistic infections
    • immunosuppression
    • change in site of microbe
    • broad spectrum antibiotic
      • yeast side effect
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19
Q

Lymphoid organs

A
  • primary - where immune cells are made and mature. bone marrow and thymus
  • secondary - mature cells encounter pathogens and antigens
  • nodes - lymphatic merge, immune cells filter and detect pathogens
    • where the immune response starts
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20
Q

lymph

A
  • fluid, oxygen, nutrients, collect waste
  • vessels - can transport pathogens, cancer cells, dead cells
  • muscles contract to circulate lymph
  • detect pathogens when in the nodes
  • W. bancrofti causes elephatitis and blocks lymphatics
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21
Q

7 innate immune cells

A
  • neutrophils - most abundant WBC
  • dendritic cells - can present antigen, phagocytic
  • macrophage - v. large, presents antigen, phagocytic
  • basophils, eosinophils, mast cells - allergic response and release histamine
  • natural killer cell - directly kill infected host cell
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22
Q

PRRs detect PAMPs

A
  • PRRs are PAMP specific
  • different receptors for different patterns
  • extracellular PRRs - on surface of cell, none for viruses because those enter the cell
  • endosome - has PRRs for extracellular detection
    • for dsRNA but also for typical PAMPs
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23
Q

Families of PRRs

A
  • Toll like recptors (TLRs) - first discovered and best studied
  • C-type lectin receptors (CLRs) - recognize CHO
  • NOD like receptors (NLRs) - free floating in the cytoplasm
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24
Q

Phagocytosis

A
  • PRR detects PAMP
  • pseudopods extend to engulf the pathogen
  • pathogen trapped in the phagosome
  • phagosome fuses with the lysosomes and granules
  • pathogen degraded in the phagolysosome
    • uses lysozyme, defensins, low pH, ROS
  • parts of pathogen are exocytosed
    • can amplify response and activate other immune cells
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25
Q

killing in the phagolysosome

A
  • oxygen dependent - ROS
    • oxidative burst to make ROS
  • pathogens with superoxide dismutase and catalase can convert ROS to H2O2 then water and O2. Avoid killing
  • Oxygen independent - low pH, defensins, enzymes
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26
Q

opsonins

A
  • complement - small proteins
    • bind to conserved pathogen components (cell wall)
  • Antibodies - bind to specific antigens
    • anti capsule antibodies
  • opsonins make the pathogen larger and easier to detect
  • receptors on phagocytes recognize opsonins and leads to phagocytosis
  • opsonophagocytosis
  • harder to opsonize a capsuled bacteria
  • back up system if PRRs dont work
27
Q

Evasion from phagocytosis

A
  • capsule - hides PAMPs from PRRs, blocks opsonins
  • catalase and superoxide dismutase to quench ROS
  • prevent formation of phagolysosome to prevent merging
  • avoid low pH by blocking the H+ pumped into phagosome
  • inhibit degradative enzymes - lysozyme and defensins
  • flagella - chemotax away
  • mutate PAMPs
  • coat in host protein to look like “self”
  • produce enzymes that degrade opsonins
  • Listeria moves from one cell to another using actin
28
Q

When neutrophil cant phagocytose

A
  • NETosis
  • Neutrophil Extracellular Trap
  • Antimicrobial peptides
  • degrading enzymes
  • kill or sequester pathogen
  • Web of DNA traps the pathogen
  • used for large microbes
29
Q

DAMP

A

danger associated molecular pattern

30
Q

NK cells

A
  • can kill infected host cells
  • all nucleated cells express MHC I protein
    • major histocompatibility complex
  • healthy cells express MHC I loaded with self protein
  • signal from healthy cell prevents NK cell from being activated
  • loss MHC I from cancer and viral infections - no MHC to activate the inhibitory receptor
  • use granzyme and perforin
  • activated from inhibitory receptor is not stimulated
    • detects missing MHC I
  • also has a NKR that binds to a ligand on the host cell
31
Q

Evade NK cells

A

force host cell to produce fake MHC

mock inhibitory receptor

32
Q

Cytokines

A

autocrine - produce cytokine to activate itself

paracrine - stimulates near by cells

endocrine - circulated befoer stimulation of other cells

chemokine - subtype that enduces cell movement

33
Q

Tissue Damage - Inflammation

A
  • dead cells release cytokines
  • resident immune cells respond
    • mast cells - histimine, vasodilator
    • macs and DCs - phagocytosis
    • bradykinin - pain
    • chemokines - recruit neutrophils
  • capillaries more permeable and cells can enter tissue
  • redness, pain, heat, swelling
34
Q

Extravasation

A

neutrophils from blood into tissues and move to highest IL-8 concentration

follow chemokine gradient

neutrophils destroy pathogen

innate cells communicate to adaptive cells that a pathogen was detected

35
Q

Innate to adaptive communication

A
  • DC and mac cells are APC (antigen presenting cells)
  • phagocytosis then present antigen on MHC II via the MHCII-antigen complex
  • produe cytokines (paracrine)
  • Helper T cell - T cell receptor (TCR) binds the antigen on the APC and activated by cytokines from phagocytic cell
  • Helper T cell activated
  • this bridge occurs in the lymph nodes
36
Q

Helper T cell

A
  • Activated by APC and cytokines
  • autocrine to stimulate clonal expansion of T helper cell
    • T helper effector - kill the pathogen now
    • T helper memory - remember pathogen for later. vaccinations
    • swollen lymph nodes
  • paracrine to B cells and killer T cells
37
Q

B cells

A

made in the bone marrow

only cells that produce antibody

antibodies are opsonins

effector and memory B cells - memory used in vaccines

each has one specific receptor (BCR)

regognizes a unique antigen

can directly bind to free floating antigens - then activated

38
Q

Killer T cells

A

aka cytotoxic T cells (CTC)

kill infected host cells

perforin and granzyme

adaptive cells

have a T cell receptor

have memory - vaccines

39
Q

Functions of B cells

A
  • neutralization - make incapable of binding to the target cell. then phagocytosis
  • agglutination of microbes - easier to detect large cluster. phagocytosis
  • Opsonization - antibodies are opsonins, leads to phagocytosis
    • antibodies can lead to holes in the membrane - lysis
  • precipitation of dissolved antigens and deactivates them
40
Q

HIV

A

infects and destroys T helper cells

lose entire adaptive immune system

41
Q

B cell activation

A
  • Need cytokines from T helper AND antigen binding to BCR to be activated
    • specific surface receptors
  • clonal expansion - new cells have the same BCR
  • BCR becomes antibody when not attached to the B cell
    • small size for dissemination
  • effector B cells aka plasma cells - secrete Abs
  • memory cells - for later response
42
Q

Cytotoxic T cell (CTL)

A

-killer T cell

  • recognize viral antigen on host cell
    • does not recognize Self protein
  • amplified by parachrine cytokines from helper T cell
  • adaptive arm
  • TCR recognizes viral Ag on host cell MHCI
    • host cell is NOT an APC
  • uses perforin and granzyme
43
Q

NK vs CTL

A
  • NK recognizes absence of MHCI self Ag
  • NK no memory, CTL has memory
  • both use perforin and granzyme
  • CTL stimulated by TH cytokines. NK no cytokines
  • TCR vs PRR
  • NK innate and CTL adaptive
  • NK responds to absence of self Ag, CTL responds to presence of viral Ag
44
Q

how to get microbiome

A
  • breast milk
  • vaginal and C section birth
  • f
  • f
  • f
  • f
45
Q

What does the microbiome do?

A
  • Co aggregation - clump pathogen so they cant bind
  • Produce biosurfactants
  • produce H2O2 and bacteriocins - kill pathogens
  • inhibitory signals
  • competitive exclusion - take up space
  • immunomodulation (alter response to the appropriate level) - immune education
  • modulate tight juctions
46
Q

anaerobes on skin

A

aerobic bacteria can consume the oxygen to a great enough extend where anaerobes can persist

47
Q

Perturb the microbiota

A
  • sexual intercourse
  • diet
  • antibiotics
  • hand sanitizer
  • age/hormones
  • fecal transplants
  • prebiotics - food for microbes
  • probiotics - good microbes
  • environment and living conditions
  • pregnancy
  • stress
  • infection
  • smoking
  • travel
  • other medication
48
Q

Site specific diversity

A

microbe diversity changes based on area of the body

49
Q

Effect of antibiotics and travel on microbiota

A
  • Antibiotics kill good and bad microbes. Very low diversity while antibiotics are in use. Then few grow back, but may develop a different diveristy/population
  • Travel - can kill of some bacteria. Different bacteria may become predominant
50
Q

Autoimmune disease

A
  • not caused by a pathogen
  • immune system targets self components and attacks the host
51
Q

Autoimmune diseases and development and helminths

A
  • helminths are most common in underdeveloped countries
  • autoimmune diseases are most prevalent in developed countries
    • suggest that lack of exposure to helminths increases risk of autoimmune diseases
52
Q

Hygiene Hypothesis

A
  • lack of early childhood exposure to infectious agents, microbes, and parasites increases susceptibility to allergic and autoimmune diseases by modulating immune system developent.
  • exposure to commensals not pathogens
  • effected by imprinting events
53
Q

Imprinting events

A
  • events exposed to commensals before age 2
  • educate the immune system
  • farm animals
  • sterility of environment - food and water
  • breast feeding
  • less antibiotics
  • siblings
  • day care
  • vaginal and c section
    • helminths
54
Q

Nonimprinting events

A

frequent Dr visits - antibiotics

only child

urban lifestyle

sterile and clean environment

55
Q

Purpose of imprinting

A
  • imprinting on innate and adaptive cells
  • educate immune system
  • dampened and dont respond
  • lower likelihood of autoimmune disease
  • higher diversity of immune cells
  • non imprinted systems are hyperactive
56
Q

Effect of nonimprinting on adaptive arm

A
  • nonimprinted system will have more active innate cells
  • leads to more active adaptive cells
  • increase cytokines from APC to helper T cells
57
Q

T helper cell

A
  • naive or virgin until activated by an Ag
  • cytokine dictates what type of T cell it becomes
  • Th 1, Th 2, Th17, T regulators
58
Q

Th 1

A

needed for killing intracellular pathogens

activate CTLs and NK cells

59
Q

Th 2

A

helps kill extracellular pathogens, specifically helminths

activate goblet cells to make mucus

stimulate peristalsis to move helminth out

60
Q

Th 17

A

induce inflammation

recruit neutrophils (short life to limit inflammation)

strongly linked to autoimmune disease

MS, UC, psorisis have high Th 17

61
Q

T regulators

A

regulate

dampen or turn down the response after pathogen is gone

out compete other cells for cytokines to weaken response

62
Q

parasitic worm therapy

A
  • use pig pathogen that has a short immune response and no worm colonization
  • stimulate Th2 to increase mucus secretion
  • worm increase T reg to increase host survival and weaken immune response
  • decrease Th 17 to supress immune response
  • try to modify the molecule that causes the immune response
63
Q

ulcerative Colitits

A
  • lack finger like projections
  • mass amount of neutrophils
  • diminish mucus
  • not elastic
  • bleeds easily - weight loss, bloody and mucus stool
  • Imbalance of Th cells
    • high Th 17 - high neutrophils
    • low Th2 and T reg
    • hyperactive neutrophils
    • inflammation
    • low mucus - immune cells have more access to commendal and can increase inflammation
64
Q

Fecal microbiota transplant

A
  • used to treat C. diff - forms spores and antibiotics kill when metabolically active
  • take broad spectrum anitbiotic - lower commensals
  • C. diff spores germinate and have more spae and nutrients
  • vegetative growth
  • gut dyxbiosis - microbiome disruption
  • abdominal pain adn GI distress
  • Abx kill veg bactaria but leave spores
  • FMT may re-establish hemostasis

Microbiology (6 decks)

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