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Immunology > Defence Against Pathogens (18-21) > Flashcards

Defence Against Pathogens (18-21) Flashcards

1
Q

What tissues are mucosal?

A

respiratory tract
intestinal tract
urogenital tract
eyes

form barrier between inside and outside which is thin and can be breached easily
- needed for light eg eye
- needed for gas exchange

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2
Q

What is the structure of epithelial cells?

A

composed of enterocytes, large polar with pili on surface

tight junctions - occludins, claudins

adherens junctions - e-cadherin, linked with f-actin

desmosomes - cadherin, linked with keratin

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3
Q

How do epithelial cells respond to pathogenic infection?

A

commensals can become harmful in case of barrier compromise

epithelial cells can secrete AMPs and mucins to control microbiota
- can also activate APCs via alarmins eg damps, IL-22, IL-5

epithelial cells have TLRs on apical and basal surfaces
- also in vacuoles and NOD proteins

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4
Q

What role do paneth cells play in the gastrointestinal tract?

A
  • located in intestinal crypts
  • secret broad AMPs
  • homeostatic balance w commensals and protection from enteric pathogens
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5
Q

What role do goblet cells play in the gastrointestinal tract?

A
  • production of mucus is main function
  • cell machinery at basal end so mucus
    secreted out of apical
  • volume can expand 100x in lumen
  • production can be upregulated by IL-
    4/13
  • mucus forms a protective viscous gel

two layers:
1. outer (luminal) loose to contain bacteria
2. inner - dense and adherent to exclude bactera

can produce cytokines

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6
Q

What role do dendritic cells play in the gastrointestinal tract?

A

extend dendrites through gut into lumen
more common in large intestine (no peyers patches or M cells)
can remodel themselves to move between epithelial cells

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7
Q

What are Peyers Patches?

A

lymphoid organs in small intestine
m cell at dome peak
SED - rich in DCs, T and B cells
B cell follicles and GCs
afferent lymphatics draining to mesenteric lymph node

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8
Q

What are M cells?

A

directly translocate luminal antigens (endocytosis)
transvesicular transport
transfer to underlying APCs

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9
Q

What are mesenteric lymph nodes?

A

MLNs
collect activated DCs and T cells from throughout intestine
activated T cells migrate through the lymphatics and thoracic duct to populate systematically, can return via bloodstream

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10
Q

How are Peyers Patches involved in the immune reaction?

A

antigen uptake by DC via M cell
or
antigen loaded DC in MLN

priming of Th0 by DCs in the thymus dependent area of peyers patch
and
priming of Th0 in the MLN

exit of antigen responsive T cells from MLN via efferent lymph node to periphery

can become IgA producing factories after induction
- can be T cell depndent or independent

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11
Q

What mucosal sites are inductive and what are effectors?

A

inductive
- tonsils, bronchus and nasal associated lymphoid tissue
- peyers patched (small intestine)
- isolated lymphoid follicles (large intestine

effectors
- gut lamina propria
- respiratory epithelium
- urogenital tract
- salivary and lacrimal glands
- mammary glands

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12
Q

What is the predominant Ig isotype in mucosal tissues?

A

IgA
IgA1 in serum and IgA2 in mucosa

most abundant Ig isotype but mainly present in gut, not most populous in blood

can neutralise microbial enzymes and toxins

hinge on 1 can be cleaved by bacteria proteases, but 2 is resistant

dimer in mucosa

monomer is inflammatory and dimer is anti-inflammatory

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13
Q

How is IgA transported into the gut?

A

Iga actively transported by polymeric Ig receptor (plgR) on epithelial cells binding to the J chain

Iga exposed to harsh environments so need secretory component (SC) to stabilise

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14
Q

How do mucosal vaccines work?

A

promotes secretory IgA
most are live attenuated which mimic tropism if pathogen

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15
Q

What is means by people who are ‘wormy’?

A

individuals who are predisposed to be susceptible to infection (by helminth parasites?)
- genetic factors
- more predisposed to Th1 response than necessarry Th2??

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16
Q

What cells are primary response against helminths?

A

IL-4 and IL-13 produced by Th2 cause muscle cells to contract vigorously pushing out gut contents (including parasites) out of body

pluripotent stem cells at base of crypt, intestinal tissues are continually turning over eg goblet cells, paneth cells, enteroendocrine cells
- ‘intestinal elevator’
- speeds up in response to IL-13 via
Th2
- Th1 decreases epithelial turn over =
increased susceptibility

intra-epithelial cells differentiate into different cell types

  • goblet: steady state - mucus lubricates and forms physical barrier covering epithelium
    • MUC2 is greatly elevated during T muris infection
    • MUC5ac is required for expulsion of T muris
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17
Q

What cells are important in the secondary response against helminths?

A
  • eosinophils: release cytokines involved in muscular contractions. degranulation
    • mMCP-1 released upon degranulation, opens up tight junctions between epithelial cells → increases fluid leaking into gut which pushes away parasites = weep and sweep

IL-5 essential for development of eosinophils

Ab-Ag cross-linking results in ADCC

eosinophils important for helminth killing during stage where it migrates to another tissue

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18
Q

Taking away helminths from population is linked to higher rate of IBD and chrons?

A

this is because they have wide range of immunomodulatory molecules which regulates our immune system
hygiene theory

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19
Q

How do helminths prevent Ag presentation?

A

inhibit APC maturation
- reduce MHC class II expression
- reduce T cell co-stimulation

apoptosis of APC (and T cells)
- filarial nematodes

desensitise PRRs
- ‘hide in plain’ site mechanism

inhibit antigen processing by the APC
eg CPI-2

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20
Q

How do helminths redirect the immune response?

A

Th2 response required to drive effector mechanisms that expel parasite from intestine

Helminths produce IFN-gamma and TGF-beta homologues

IFN-gamma blocks T cell differentiation into Th2, instead promotes differentiation into Th1

21
Q

How do helminths disarm the immune response?

A

ADCC
- serpins inhibit protease activity

AD respiratory burst
- anti-oxidants inhibit this

immune cell recruitment
- hookworm protease degrades eotaxin produced by eosinophils

22
Q

What are protozoa?

A
  • complex life cycles often w intracellular and extracellular stages
  • single celled
  • free living or parasitic
23
Q

What is the life cycle of malaria in humans?

A

spread by female anopheles mosquitoes

sporozoites rapidly migrate to liver and enter hepatocytes and mature into schizonts , which rupture and release merozoites

mature into trophozoites in blood

symptoms show during blood infection stage, stronger immune response than in liver

24
Q

What is the lifecycle of toxoplasmosa gondii?

A

definitive host is cat
intracellular parasite
forms oocysts containing protozoa which remain viable for years
- poorly immunogenic
opportunistic infection, cysts may reactivate

can be passed from mother to infant
if passed on during first trimester, can cause stillbirth

25
Q

What is the lifecycle of leishmania spp>

A

transmitted by female sandflies

obligate intracellular parasite that primarily invades macrophages

infected cells taken up by flies and transferred to another host

many different species, give rise to different types of disease

26
Q

What is the trypanosoma spp life cycle?

A

transmitted by triatomine bug (T cruzi), south and central america
or tsetse fly (T brucei), africa

cruzi require nucleated cell to undergo asexual reproduction
brucei can asexually reproduce in circulation

27
Q

What is the most important factor in the immune response against protozoa?

A

recognition of parasite is key process in activation of immune response
PRRs recognise protozoan PAMPs
eg
GPI - used to attach proteins to cell surface for adhesion and molecule trasnport

genomic DNA

haemozoin - inorganic crystal biproduct of haemoglobin digestion by plasmodium

PFTG - protein that faciilitates cell movement and cell invasion by toxoplasma

28
Q

In the context of protozoa, what is the result of TLR stimulation?

A

production of anti inflammatory cytokines (IL-10, TGFb) in response, to prevent excessive immunopathology and aid parasite persistence

induction of ROS in macrophages
upregulation of co-stimulatory receptors to stimulate the adaptive immune response

Myd88: TLR adaptor protein myeloid differentiation primary response gene 88 – downstream of all TLRs except TLR3

  • TLR signalling through MyD88 is necessary to control many protozoan infections
29
Q

What types of macrophages are there and what are their abilities to phagocytose pathogens?

A

M1- classically activated
- highly phagocytic

M2 - alternatively activated
- reduced phagocytosis

30
Q

How does Leishmania live inside macrophages?

A

uses LPG to
- delay fusion of phagosome w lysosome
- protect from ROS and NO damage
- inhibit inflammatory cytokine production eg IL-12

31
Q

What is the role of neutrophils in response to protozoan parasites?

A

recruited by chemokines and activated through cytokines and PRRs
ROS/NOS production and release of proteolytic enzymes and extracellular NETs
LPG in Leishmania induces NET release

even if sandfly does not have leishmania, a bite will still cause neutrophils to be recruited to site as DAMPs are released and antigens in saliva

32
Q

What is the role of DCs in response to protozoan parasites?

A

upregulation of CD80, 86, 40 producing proinflammatory cytokines such as TNFalpha and Il-12

protozoan parasites subvert innate immune response by modulating DC effector mechanisms
can inhibit maturation of DCs, therefore dont travel to lymph node and activate T cells

33
Q

How do T cells provide immunity during different stages of malaria infection?

A

CD8 T cells provide immunity during the liver stage of malaria infection and CD4 t cells protect against blood stage

liver cells do not express MHC II
blood cells do not express MHC I or II

blood passes through spleen and macrophages engulf infected blood cells

34
Q

How are B cells important in malaria infection?

A

takes a while for antibodies to form, most are IgM and takes time to class switch to IgG

in secondary response, much quicker antibody producion and almost all are IgG

production of antibodies and class switching are crucial to handling malaria infection, especially on repeated infections

35
Q

How do trypanosomes evade humoral responses?

A

changing of variant surface glycoprotein coat (VSG) every few weeks means it is always ahead of host immune system

36
Q

How do bacteria cause disease?

A
  1. toxin release or attachment to epithelial surfaces without invasion
    eg diptheria toxin
  2. invasion of tissue or cells leading to physical damage (DAMPS) or stimulating immunopathology (PAMPS)
  3. a mixture of 1 and 2
37
Q

What immune mediated pathologies are caused by bacteria?

A
  1. sepsis/septic shock
  2. super antigens
  3. rheumatic fever
    - cross reaction of antibodies

when a superantigen (eg staph enterotoxin B) binds, it binds outside of groove on TCR (eg Vbeta3) meaning it is activated

any TCR with that receptor will be activated causing a huge cytokine strom and mass activation of other cells

38
Q

How do the bacterial cell walls influence immunity?

A

gram positive has thick wall of peptidoglycan, large resistance to bile
also has capsular polysaccharide, protection agaisnt desiccation and host recognition (complement)

gram negative has LPS on outer membrane - major toxin

39
Q

How do CD4 and CD8 T cells co-operate to kill intracellular bacteria?

A

Th1 cells enhance macrophage killing via IFN-gamma
CTL kill infected cells in which bacteria have evaded phagocytosis

40
Q

How is the complement system effective against viral infection?

A

classical activation through direct binding to viruses eg HIV and dengue virus

the MBL proteins of the lectin pathway can interact w numerous viral carb antigens

many viruses target complement eg HIV incorporates CD55 and CD59 into its membrane ans encode secreted proteins that block C3 convertase activity

41
Q

What are some antibacterial roles of antibodies in realtion to different aspects of bacterial virulence?

A

attachment: antibodies attach to fimbriae, capsules, lipoteichoic acid

proliferation: block of transport systems eg for iron
trigger compliment to damage gram- outer membrane

avoiding phagocytosis: neutralise immunorepellents
bind to M proteins and capsule - opsonise via Fc and C3 receptors

damage to host: antibodies neutralise toxins and spreading factors eg hyaluronidase

42
Q

How do innate cells recognise viruses?

A

intracelllular PRR ligation
eg TLR-3 which recognises dsRNA or TLR-7 which binds ssRNA, both in endosome

this activates interferon regulatory factors (IRF3/7 respectively) (TFs)

leads to production of type I interferon cytokine production

43
Q

How do innate cells respond to viral infection?

A

receptor for type I IFNs = heterodimer, IFNAR1 and IFNAR2

causes JAK-STAT signalling (STAT1 and STAT2)

activates interferon regulatory factor IRF9

causes transcription of interferon response genes (ISGs)
- induce resistance to viral replication in all cells
- increase MHC I expression and antigen presentation in all cells
- activate DCs and macrophages
- activate NK cells to kill virus-infected cells

may signal other cells (paracrine) or back onto itself (autocrine)
shutoff of host cell protein synthesis is temporary, too long and causes damage to own cells, but enough time for immune to kick in

44
Q

What role do NK cells play in killing viruses?

A

NK cells function is regulated by balance between inhibitory and activating receptors

inhibitory receptors recognise MHC class I molecules

during viral infection, viruses downregulate MHC I to avoid CTL recognition and killing

this removes inhibitory signal of NK cells and they are targeted

some viruses can create MHC class I mimics to prevent NK cell detection

45
Q

What are some methods of antibody mediated host pathology?

A

a. antibody-mediated viral neutralisation

b. antibody-dependent enhancement (ADE) of infection

c. ant-body-mediated immune enhancement

in rare cases ADE promotes entry of viruses into FcR expressing cells -> spread of infection

viruses inside macrophages can also encounter TLRs that induce inflammatory (IFN-gamma) response - if happens in lung = bad

46
Q

How do virus genetics allow evasion of the immune system?

A

viruses replicate rapidly and prone to random mutations = antigenic drift between generations

influenza has antigenic shift, allows evasion from antibodies
- 8 separate ssRNA segments which can undergo reassortment in cells infected w two strains -> novel viral antigens

47
Q

How are viral antigens processed and presented?

A

Protein Degradation:
Viral proteins are broken down into smaller peptides by the proteasome in the cytoplasm.

Transport to Endoplasmic Reticulum (ER):
these peptides are transported into the endoplasmic reticulum (ER) by transporter proteins, such as TAP (Transporter associated with Antigen Processing).

Loading onto MHC Class I Molecules:
In the ER, peptides are loaded onto newly synthesized MHC class I molecules that have just been assembled within the ER.

Transport to Cell Surface:
MHC class I molecules loaded with viral peptides are transported from the ER through the Golgi apparatus to the cell surface.

Presentation to Immune Cells:
The MHC class I molecules on the cell surface present the viral peptides to CD8+ T cells (cytotoxic T lymphocytes or CTLs) for immune recognition and are killed via perforin and granzyme action
or Fas/FasL

48
Q

How do viruses block Fas/FasL killing?

A

block the formation of the death domain which is needed for recruitment and activation of procaspase 8 -> apoptosis

Immunology (5 decks)

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