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cellular parasitology > Vl 5 - Plasmodium host cell interaction > Flashcards

Vl 5 - Plasmodium host cell interaction Flashcards

1
Q

what are the properties of the innate immunity?

A
  • unspecific
  • instantanious reaction
  • no memory
  • reacts to reinfection in the same way as first infection
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2
Q

what are the properties of acquired immunity?

A
  • specific
  • delayed
  • memory, immunity against reinfection
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3
Q

How does pre-erythrocytic immunity against plasmodium work?

A
  • sporozoites in skin: T-cell priming, antibody response
  • sporozoites in spleen: priming of CD8 T-cells
  • liver stages: Toll like receptor + priming and effector mechanism T-cells (NK-cells + CD8/CD4-T-Cells)
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4
Q

What is the function of the plasmodium cysteine-protease? How is it inhibited by the immune system?

A
  • cleaves CSP ⇒ adhesion+invasion

- B cell priming in the skin ⇒ cysteine protease blocked by antibody, no cleavage ⇒ adhesion blocked

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5
Q

how is anti-blood stage immunity induced?

A
  • antibody response, infected RBC sequestion

- elimination of infected red blood cells by spleen

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6
Q

How does the immune system inhibit of merozoites?

A
  • attaching antibodies ⇒ phagocytosis
  • complement deposition ⇒ phagocytosis or lysis
  • invasion blocking antibodies
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7
Q

other strategies of immune system

A

complement fixation, invasion inhibition
phagocytosis: monocyte
respiratory burst: neutrophile
antibody-dependent cellular inhibition: monocyte

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8
Q

How do infected red blood cells avoid splenic clearance?

A
  • knob formation (PfEMP1) ⇒ cytoadherence to endothelium cells ⇒ rosetting (STEVOR and RIFIN mediate rosetting)
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9
Q

To what extent does antigen recognition differ between T and B cells?

A

T cells: Presentation of antigen fragments via MHC-I (all nuclear cells) and MHC-II molecules (dendritic cells and mononuclear phagocytes). Recognition via TCR. + Additional signals ⇒ Naive TH cell is activated and differentiates.

B cells: recognition of antigen via own AB
- differentiate to plasma cells (can produce and secrete more AB)

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10
Q

Which cell types can naive T cells differentiate into?

A

TH1: Cell-mediated immune response: activation of phagocytes, NK cells, cytotoxic T cells. Against intracellular parasites.

TH2: Humoral immune response: AK. Against extracellular parasites.

Treg: Immunosuppression tolerance ⇒ regulate immune response (prevent autoimmune response)

TH17: Inflammation: Induce body cells to produce chemokines and cytokines. These attract granulocytes (but also NK cells, DCs and macrophages) that fight bacterial pathogens.

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11
Q

How does the body react to Plasmodium with regard to the immune response?

A
  • sporozoites injected in skin ⇒ antibodies formed in nearest lymph nodes + T-cells primed
  • some sporozoites cross spleen before entering the liver ⇒sporozoite enters the white pulp ⇒ AG is absorbed by CD8+-DC cells and presented via MHC-I an (cross presentation) to CD8-T cells that are primed (adaptive immune response) ⇒ These migrate into the liver.
  • sporozoites invade liver (immune-privileged) ⇒ silent immune response (but priming and effector mechanisms)
  • merozoites released into blood vessels ⇒
    AB formed + CD4+ T-cells (Th1 cytokines; regulatory cytokines) + macrophages
  • killed via phagocytosis (monocytes) or respiratory burst (neutrophils)
  • AB against PfEMP1 from Plasmodium on RBC surface ⇒ recognized and eliminated by spleen (evasion through PfEMP1)

During the entire process, T cells are primed in the skin, spleen and liver ⇒ In second infection (or immunized mouse) much more T cell recruitment

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12
Q

What are the most important plasmodium antigens?

A
  • TRAP and CSP (Circumsporozoite Protein)
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13
Q

What happens when sporozoites remain in the skin?

A
  • penetrate into cells and form EEFs ⇒ absorbed by DCs and macrophages
  • DC presented in the spleen (white pulp) or in the nearest lymph node AG to CD4- (via MHC-II) and CD8-T-cells (via MHC-I)
  • CD 8 proliferates and migrates into the liver.
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14
Q

What is the parasitic CS protein needed for? Which of these functions can be stopped by antibodies?

A
  • formation of sporozoites
  • Sporozoites leaving oocysts
  • Salivary gland invasion
  • Gliding motility (AB)
  • hepatocyte invasion (AB)
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15
Q

What happens during a Plasmodium infection when mice have previously been immunized with irradiated sporozoites?

A
  • Sporozoites less motility, BUT formed antibodies not able to slow down all sporozoites.
  • antibodies bind nonadhesive CSP, which prevents the cysteine protease CSP from cleaving it (needs to be cleaved for adheasion and invasion of hepatocytes)
  • Formed AB can also strip off the CSP coat of the sporozoites -> no liver invasion possible
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16
Q

How does Plasmodium enter the liver?

A

Sporozoites attach to stellate cell and migrate until they recognize Kupffer’s cells ⇒ traverses Kupffer’s cells and wanders through several hepatocytes (are all damaged by this)
- penetrates a cell after formation of a parasitophore vacuole

17
Q

How does the induction of the immune response occur in the liver stage? What are the effector immune mechanisms against Plasmodium pre-erythrocytic stages?

A
  • before entering hepatocyte:
    antigens recognized by Toll-like rec. (TLR) ⇒
    NF-κB and NO production
  • priming of CD8-T-cells in spleen
  • invaded hepatocytes and the ones that are wounded by traversing sporozites present antigen via MHC-I to CD8-T cells OR activate DCs ⇒ induction of specific CD4+ and CD8+ T cell responses
  • CD4+ and CD8+ T cells can eliminate intracellular parasites either directly by cytolysis or indirectly by the production of IFN-γ (central immune response) ⇒ NO production
18
Q

Which proteins do T cells need for their rapid movement? What happens to the T-cells after the organism is immunized?

A
  • ICAM-1 and ITGAL

- After vaccination, many CD-8 T cells patrol along the liver ⇒ but diminish with time

19
Q

What mechanisms are used against plasmodium blood stages? Which mechanisms do not take place among others

A
  • antibody response, sequestration of infected RBC and elimination of infected RBC by the spleen
  • RBCs no nuclei and therefore no antigen presentation ⇒ no T-cells are primed
20
Q

What immunevasion strategy do merozoites use to survive in the blood?

A
  • Sequence of Plasmodium-OFP varies but function is maintained (⇒ MSPs, AMA1, EMP1)
  • Redundancy of multi-gene families (EBAs, RHs)
  • Reduced antigenicity (RH5)
21
Q

How does replication in the RBC work?

A

1) Merozoite enters erythrocyte
2) develops to early ring stage (parasitic proteins are produced and transported to erythrocyte surface)
3) ring develops to intermediate trophozoite stage
4) trophozoites develop to mature schizont stage
5) shizont cleaveses itself
6) merozoites lyse the cell

22
Q

Which proteins have a strong affinity for PfEMP1?

A
  • surface receptors on ephitel cells (EC)
  • CD36, EPCR, PECAM-I and ICAM-I

in cerebral malaria:
- DC8 and DC13 (PfEMP1 subunits) bind EPCR, DC5 binds PECAM-1 and DC4 binds ICAM-1

23
Q

In which cases can an adult who shows no or hardly any malaria symptoms again show a strong immune response? Why?

A
  • In case of pregnancy
  • Pregnancy-associated malaria is an organ-specific syndrome triggered by the expression of the PfEMP1 variant VAR2CSA ⇒ mediates IE binding to placental CSA
24
Q

What bad clinical pictures can a severe malaria show?

A
  • high fever due to synchronized proliferation and antigen excretion
  • anemia due to rupture of erythrocytes
  • cerebral malaria by clogging up blood vessels in brain region
  • multiple organ failure
25
Q

What are the different functions of the white and red pulp in the spleen?

A
  • white pulp used for immune defence, constantly checks the blood flow for antigens and toxins
  • colonized by B- and T-cells
  • red pulp: outdated or abnormal RBC are destroyed (by macrophages)
26
Q

what is priming of immune cells?

A
  • first contact of naive B-or T-cells with presented antigen
27
Q

liver stage priming

A
  • before sporozoite enters hepatocyte: excreted antigens recognized by toll like receptors ⇒ can induce NF-κB and NO production, killing the exoerythrocytic form (EEF) of plasmodium
  • sporozoite inside hepatic cell: cell can present antigen to CD8 T-cells via MHC1 and CD4 T-cells via MHC2, can also induce IFNy production⇒ NO production

cellular parasitology (10 decks)

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