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Immunology Final Exam > Immunity to Pathogens > Flashcards

Immunity to Pathogens Flashcards

1
Q

Infection

A

-the process by which pathogens enter into a harmful, selfish relationship with the host organism

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2
Q

Immune Response to Pathogens

A
  • successful invasion of the host by a pathogen and establishment of an infection require that the pathogen overcome innate and adaptive immunity
  • pathogenesis is often caused by the hosts immune response rather than direct tissue damage caused by the pathogen or its toxins
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3
Q

Antiviral Immune Responses

A

-innate immunity to viral infections is largely through the induction of type I interferons (IFNalpha/beta) via TLRs that detect viral dsRNA in infected cells and nearby uninfected cells

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4
Q

IFN alpha/ beta receptor signalling

A
  • induces the Tc of Mx proteins that inhibit virus Tc and assembly
  • Rnase L that degrades viral mRNA
  • dsRNA dep. protein kinase R that block protein TL
  • IFNalpha/beta also bind IFNalpha/beta receptor on NK cells inducing lytic activity which is furthur enhanced in the presence of IL12 produced by innate immune cells (e.g. dendritic cells)
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5
Q

Antibodies contain the spread of viruses and protect against reinfection by: (4)

A
  1. blocking viral attachment to host cells (esp. secretory IgA)
  2. preventing fusion of the viral envelope w/ host cell membranes
  3. agglutination and opsonization of viral particles for removal by phagocytes (Igm, dimeric IgA, IgG)
  4. activation of the classical complement pathway-results in opsonization of viral particles by C3b and lysis of enveloped virus by the membrane attack complex
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6
Q

Cell-mediated viral clearance

A
  1. IFNgamma secreted by CD4+ Th1 cells and CD8+ CTL has direct antiviral activity
  2. CTL (activated by Th1 produced IL2) target and kill virus infected cells, thereby eliminating the source of new infection
  3. NK cells (activated by IFNgamma, IL2) are directly lytic for virus infected cells and can also kill by antibody dep. cell mediated cytotoxicity (ADCC)
  4. macrophages that are activated by IFNgamma can kill virus infected cells by ADCC
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7
Q

Viral Evasion of Immune Responses-protein kinase R

A

-evading the action of IFNalpha/beta by blocking/inhibiting the action of dsRNA-dep protein kinase R (eg. hep C)

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8
Q

Viral Evasion of Immune Responses-Inhibition of viral antigen presentation

A
  • by down reg of class I MHC expression (e.g. adeno)
  • inhibiting the transporter molecule (TAP) needed for antigen processing (HSV)
  • some viruses reduce classII MHC expression by APC, preventing activation of T helper cells (CMV)
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9
Q

Viral Evasion of Immune Responses-Alterations in viral antigens

A
  • constant alteration in viral antigens by antigenic drift/shift
  • point mutations in viral genome (drift)
  • exchange of genetic material w/ viral reservoirs in other hosts (shift)
  • prevents development of a secondary immune response (memory B cells generated during primary infection cannot be used)
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10
Q

Viral Evasion of Immune Responses-Interfering w/ Complement

A
  • HSV1 produces a C3 binding protein that increases the decay of C3 convertase, inhibiting the alternative pathway of complement activation
  • vaccinia secretes a C4b binding protein that inhibits the classical pathway of complement activation
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11
Q

Viral Evasion of Immune Responses-Capping and shedding

A

-modulation of viral antigen from the surface of infected cells by capping and shedding following antigen interaction w/ virus specific antibody allows measles virus infected cells to escape destruction by virus infected cells

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12
Q

Viral Evasion of Immune Responses-Suppresion of antiviral immune response

A
  • activating reg T cells (measles)
  • altering the Th1/th2 cytokine balance (EBV codes for IL10 like molecule)
  • destroying essential lymphoid tissues (HIV destroys lymph node architecture)
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13
Q

Immune Response to Infection by Extracell bacteria

A
  • bacteria invade the body through mucosal surfaces or breaks in the skin
  • infection requires attachment to host cells, proliferation of bacteria, invasion of host tissue, toxin induced damage to host cells
  • low level infection can be controlled by the innate response (primarily phagocytosis by neutrophils ) while higher levels of infection require the adaptive immune response for clearance
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14
Q

The role of antibody in response to infection by extracellular bacteria

A
  1. prevent attachment/colonization (secretory IgA)
  2. neutralize bacterial exotoxins/endotoxins
  3. act as an opsonin to enhance phagocytosis
  4. activate complement by the classical pathway, resulting in the lysis of gram negative bacteria by mac
    - prod of C3b (opsonin), C3a, C5a (anaphylatoxins) that cause mast cell degranulation, leading to vasodilation, extravasation of leukocytes into the infected tissue
    - chemotactic factors produced by mast cells (neutrophil chemotactic factor) and by complement degradation (C3a, C5a, C5b67 are chemotactic for neutrophils and macrophages)
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15
Q

Bacterial Evasion of Immune Responses-Cell surface structures

A

-production of cell surface structures (pili, adhesion molecules) that enhance the ability of bacteria to attach to the mucosal epithelium

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16
Q

Bacterial Evasion of Immune Responses-proteases

A
  • secretion of proteases that cleave secretory IgA at the hinge region
  • reduces the half life of secretory IgA in mucosal secretions
  • prevents IgA mediated agglutination of bacteria
17
Q

Bacterial Evasion of Immune Responses-changes in aa sequence

A

-continual changes in the aa sequence of key surface structures such as pillin (the protein component of pili) allow bacteria to evade the IgA response

18
Q

Bacterial Evasion of Immune Responses-Inhibtion of phagocytosis

A
  • expression of surface structures (e.g. polysaccharide capsule, M protein) that inhibit phagocytosis
  • batcerial toxins can interfere w/ phagocytosis by poisoning and killing leukocytes
19
Q

Bacterial Evasion of Immune Responses-Interferance with Complement System (4)

A
  • poor activation of the alternative complement pathway due to the synthesis of capsules that fail to stabilize C3 convertase (C3bBb)
  • resistance to the mac due to the presence of capsules/thick peptidoglycan that prevent the insertion of terminal complement components
  • complement activation site deviation by secreted decoy proteins or bacterial surface proteins that are distal to the cell surface
  • acceleration of complement breakdown by secreted enzymes
20
Q

Immune Response and Pathogenesis

A

-immune response to extracellular bacteria can contribute to pathogenesis of bacterial infections by the overproduction of septic shock inducing IL1, TNFalpha in response to cell wall endotoxins of gram negative bacteria

21
Q

Intracellular bacteria colonize phagocytic cells (esp. macrophages) by: (3)

A
  1. inhibiting lysosome fusion (Mycobacteria)
  2. resisting oxidative/lysosomal attack (Mycobacteria)
  3. escaping the phagosome following phagocytosis (Listeria)
22
Q

Immune Response to Intracellular bacteria

A
  • cell mediated immunity (DTH response) protects against intracellular bacterial infections
  • Th1 cells (and to a lesser extent CTL and NK cells) release IFNgamma that activates macrophages, increasing their phagocytic activity and killing of phagocytosed microbes, enhances class II MHC expression and antigen presentation
  • CTL (activated by IL2 from Th1 cells) kill infected macrophages, releasing bacteria, which are then phagocytosed and killed by activated uninfected macrophages
23
Q

Immune Response to Intracellular bacteria-granuloma

A
  • if infection by intracell bacteria persists, the chronic cell mediated immune response leads to the formation of granuloma that isolates the site of infection
  • can also lead to tissue necrosis due to the accumulation of high local concentrations of lysosomal enzymes secreted by activated macrophages
24
Q

Infection by Parasites-Protozoa

A
  • unicellular, eukaryotic
  • multistage growth cycles that can cause disease
  • at some stages of their life cycle protozoa are extracellular but at other stages their growth is intracellular
  • humoral and cell mediated immune responses are only effective at certain times
25
Q

Infection by Parasites-Malaria

A
  • plasmodium species introduced into humans by mosquito bites
  • sporozoites from the mosquito pass through the blood to enter liver cells
  • in liver merozoites are produced and return to blood to infect RBC
  • infected RBC rupture, releasing additional merozoites, some of which become male and female gametocytes that are ingested by mosquitoes, differentiate into sporozoites
  • the sporozoite stage is only in blood for 30 mins, limiting the effectiveness of antibody response
  • during intracellular stage, protozoa only susceptible to cell mediated immunity
26
Q

Infection by Parasites-Plasmodium surface antigens

A
  • surface antigens that change as the protozoa goes through its maturational stages
  • impairs development of effective immune response
  • surface antigens that have bound antibody are sloughed off, rendering antibodies ineffective
27
Q

Infection by Parasites-Trypanosoma

A
  • causes African sleeping sickness
  • large repertoire of genes coding for variable surface glycoprotein
  • sequential expression of which allows for evasion of antibody responses
28
Q

Infection by Parasites-Helminths

A
  • large, multicellular parasitic worms
  • extracellular
  • protection is through humeral and cell mediated immunity, involves Th2 and IgE synthesis
29
Q

Infection by Parasites-Helminths: Schistoma species have evolved protective mechanisms

A
  • decresed expression of antigens on its outer membrane
  • antigen masking w/ host ABO blood group and histocompatibility antigens
  • induces a stong Th2 response in mice, protective immunity requires a th1 cell mediated response
  • the ability to stimulate the cytokine production is defense strategy
30
Q

Role of IgE in Helminth Infection

A
  • worm antigens cause IgE sensitized mast cells in the lining of the gut to degranulate
  • results in increased vascular permeability and secretion of eosinophil chemotactic factor that allows worm specific IgG and eosinophils to reach worms in the lumen of the gut
  • eosinophils then bind to the IgG coated worm via Fc receptors
  • release granule contents (major basic protein) that kills the worm
  • smooth muscle contraction caused by histamine and other mast cell secreted mediators expels the worm
31
Q

Role of IgE in Helminth Infection-activation of tissue mast cells

A

-activation by anaphylatoxins (C3a, C5a) generated by complement breakdown is also impt in induction and maintenance of acute inflammatory responses to helminthic infections

Immunology Final Exam (5 decks)

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