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immuno > Chapter 13 > Flashcards

Chapter 13 Flashcards

1
Q

Diseases are caused by inherited gene defects (congenital)
-adaptive usually but worse when it’s in innate

A

Primary immunodeficiency

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2
Q

Are acquired as a consequence of other diseases or result from other issues such as starvation or medical intervention

A

Secondary immunodeficiency

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3
Q

Primary immunodeficiency diseases are caused by inherited gene defects in ____

A

Cell development

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4
Q

Most gene defects resulting in immunodeficiency are ___and many caused by mutations in __chromosome

A

Recessive; X

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5
Q

-problem with cytokine signaling
-men are more likely to have
-women are carriers but must be on active X

A

Severe combined immunodeficiency (SCID)

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6
Q

SCID is caused by mutations in gene ____ on X. It encodes _____receptor. Mutation causes problem in signaling of?

A
  1. IL2RG
  2. IL2
  3. All IL2 family cytokines. IL2 family forces cells to differentiate into Treg
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7
Q

If _____ and _____don’t work T cells and NK don’t properly develop

A

IL7 and IL15 (needed for survival of CD4 and CD8 memory T cell; maintenance of memory)

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8
Q

Specific abnormality: Thymic aplasia
Immune defect: variable numbers of T cells
Susceptibility: general

A

Digeorge syndrome

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9
Q

Specific abnormality: mutations in TAP 1, TAP2 and tapsin
Immune defect: no CD8 T cells
Susceptibility: chronic lung and skin inflammation

A

MHC class I deficiency

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10
Q

Specific abnormality: lack of expression of MHC class II
Immune defect: no CD4 T cells
Susceptibility: general

A

MHC class II deficiency

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11
Q

What can the defects in immunodeficiency diseases be?

A
  1. Defects in T cell development
  2. Defects in signaling
  3. Defects in B cell development result in deficiency’s in antibody production that cause an inability to clear extra cellular bacteria and some viruses
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12
Q

B cell defects can lead to problems in ____

A

Class switching

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13
Q

-born with high level of maternal ___ (moves across placenta)
-after birth, ___ starts immediately

A

IgG; IgM

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14
Q

IgG starts at ___ months; total IgG falls because maternal IgG catabolized
- IgG levels are low from ____ to ____

A

6 months; 3 months to 1 year of infant

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15
Q

In males stimulation of the pre B-cell receptor recruits cytoplasmic proteins including ____ to transduce a signal that triggers B cell development.

A

BTK (Brutons tyrosine Kinase)

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16
Q

In males the X-linked agammaglobulinema (XLA) the ____ gene on X chromosome is defective

A

BTK protein

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17
Q

-tyrosine protein
-IgM will only have BTK signal transduction

A

BTK protein

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18
Q

In male with XLA ___ signal transduced even though receptor is there

A

no

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19
Q

In females half of the pre-B cells will have be expressing the defective BTK gene and will not develop further. This is since one of the two X chromosomes in each cell is ______ early in development

A

permanently inctivated

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20
Q

Defects in activationand differention will have an impact on cell mediated and ____ response

A

antibody

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21
Q

defects specific to activation and differentiation of B cells can impair their ability to do _____ and leave cell mediated response intact

A

class switching IgG, A, or E

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22
Q

Common feature of patients with defects in B cell class switching is ____. have normal B and T cell development and normal or high serum IgM, but make limited antibody response that require T cell help

A

hyper-IgM syndrome

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23
Q

In this syndrome you can not class switch, have build up of M and long term immunity is effected because you can not make IgG

A

hyper-IgM syndrome

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24
Q

In X-linked hyper IgM syndrome: mutation in ______. This is on activated T cells allowing them to engage with CD40 antigen presenting cells.
-patients have severely reduced circulating antibody levels of all except IgM and are highly susceptible to bacterial infections

A

CD40 Ligand

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25
Q

In males with hyper-IgM syndrome in the CD 40 Ligand the B cells are normal, But ________.

A

dont engage with T cells, dont undergo isotype switching or intiate the formation of germinal centers

26
Q

Can have inherited defects in signaling pathways CD4 T cells
-Normal pathways for host defense against different infectious agents are pinpointed by genetic deficiencies of cytokine pathways central to _____ and ___ responses
-defects are not in antibody production, but in the ____ pathways.
-such defects make them susceptible to some bacterial infections

A
  1. Type 1/TH1 and Type 3/TH17
  2. signaling
27
Q

can have inherited defects in signaling pathways (CD8 T cells)
-inherited defects in the cytolytic pathway of lymphocytes can cause uncontrolled _____ and ____ responses to viral infections

A

lymphoproliferation and inflammatory responses

28
Q

while there is impaired release of sytotoxic granules, there is uncontrolled activation and expansion of CD 8 T cells and macrophages that infilitrate multiple organs, cause tissue necrosis and organ failure. _____ is released from ___ and ___ and this leads to ______

A
  1. IFN-gamma (which brings macrophages and inflammatory cytokines)
  2. CTLs
  3. NK
  4. greater activity of macrophages, and pro-inflammatory cytokines such as TNF, IL-6 and CSF
29
Q

Defects in complement components and complement regulatory proteins cause ____ and tissue daamage

A

defective humoral immune function

30
Q

In classical pathway (C1, C2 and C4) deficiency leads to ____. Antibody and antigen combine but nothing else happens.

A

immune complex diseases

31
Q

In MBL pathway (MBL, MASP1, MASP2, C2, C4) deficiency of MBL leads to ____, mainly in childhood

A

bacterial infections

32
Q

In the alternative pathway (Factor D and Factor P (regulate complement)) deficiency leads to infection with pyogenic bacteria and Neisseria spp. but ____

A

no immune complex disease (more genetic problems in the human being)

33
Q

___ deficiency leads to infections with pyogenic bacteria and Neisseria spp. sometimes immune complex disease

A

C3

34
Q

membrane attack components (C5, C6, C7, C8, C9) deficiency leads to infection with ____ only

A

Neisseria spp.

35
Q

_____ or gene therapy can be useful to correct genetic defects

A

hematopoietic stem cell transplantation

36
Q

-4 different things bacteria/ virus can do to evade the immune system
1. extracellular bacterial pathogens have evolved different strategies to avoid detection by ____ and destruction by antibody, complement and antimicrobial peptides
2. Intracellular bacterial pathogens can invade the immune system by _____
3. RNA viruses use different mechanisms of ____ to keep a step ahead of the adaptive immune system
4. DNA viruses use multiple mechanisms to subvert ___ and ___ responses

A
  1. pattern recognition receptors
  2. seeking shelter within phagocytes
  3. antigenic variation
  4. NK cell and CTL
37
Q

what are the 5 ways extracellular bacteria avoids detection?

A

sheilding on MAMPs, antigenic variation, inhibition of oposonization, inhibition of ROS and resistance to antimicrobial peptides

38
Q

change the antigen so it not recognized like spike porteins

A

antigenic variation

39
Q

bacteria have capsule so makes it difficult for C3b to land for oponization

A

Inhibition of opsonization

40
Q

Intracellular bacteria evade the immune system ….
____(inside macrophages)
-tuberculosis infects lungs and manifests by coughing
-causative agent of leprosy

A

mycobacterium

41
Q

Intracellular bacteria evade the immune system ….
____(spinach) escape from phagosome into the cytoplasm of macrophage where they multiply

A

listeria monocytogenes

42
Q

Intracellular bacteria evade the immune system ….
____uses type III secretion system to secrete SifA into host cytosol and membranes to alter composition of ___ containing vacuole to avoid destruction

A

Salmonella

43
Q

In salmonella
1. Gram negative organisms have type III or type Iv secretion systems or injectisomes
2. assembly of proteins on membrane
3. bacterial proteins injected into host cell
4. these virulence factors aid in escaping inmmune response: block signaling cascade ____and ____

A

NFkB and MAP kinases

44
Q

_____ (causative agent of plaque) YOP proteins which inject into phagocytes, destroys the actin cytoskeleton, which is needed for phagocytosis

A

Yersinia pestis

45
Q

_____destroy cytoskeleton through inject system and secretion system. when the cytoskeleton is destroyed it is called Ruffle. it allows microorganisms to enter.

A

salmonella

46
Q
  1. several pattern recognition receptors that recognize microbial forms of DNA and RNA produced in the course of viral infection and replication activate the production of ___ by the infected cell
  2. heterodimeric receptors for these cytokines are expressed on nearly all cells of the body and activate ____ and ____ to amplify production of the interferons and induce expression of restriction factors that block replication of viruses
  3. Key sites in the interferon signaling cascades are blocked by many viruses
A
  1. interferons
  2. STAT 1 and STAT 2
47
Q

antigeneic changes from reassortment of segments of RNA genome leads to ____= global pandemics every 10-50 years

A

antigenic shift

48
Q

-overtime antigens change, for example influenza it changes all the time, the surface proteins are changing
-neutralizing antibodies against hemagglutinin block binding to cells
-mutations alter epitopes in hemagglutinin so that neutralizing antibody no longer binds

A

antigenic drift

49
Q

-occurs when RNA segments are exchanged between viral strains in a secondary host
-no cross protective immunity to virus expressing a novel hemagglutinin

A

antigenic shift

50
Q

DNA viruses have….
1. _____ but employ antigenic variation. Have larger genomes, more proteins that help them fight off immune cells. (herpes viruses: latency, no viral proteins loaded on MHC I)
2. ______ (viral homologs of MHC I which ends up binding NK cells and blocks its action)
3. Viral homologs of cytokines and their receptors. Decoy receptors that interfere with ___ or ______

A
  1. low mutation rate
  2. repress cytolytic activity of NK cells
  3. natural ligand signaling, or make proteins that inhibit JAK/STAT signaling
51
Q

many proteins which prevent the appearance of viral peptide : MHC I on the infected cell

A

immunoevasins

52
Q

some viral proteins degrade the newly made MHC I molecule using a pathway that usually degrades misfolded proteins

A

dislocation

53
Q

Latency of viruses
1. these viruses enter latency by expression of small region of their genome called ____
2. This suppresses the transcription of viral genome, produces factors that interfere with apoptotic host cell death, immune mechanisms that could clear death
-herpes goes latent and hides from immune system, hiding in the trigeminal ganglion. it hides in nerves because it is non dividing and it comes out in stress. herpes produces products to keep the ganglion alive and prevents the immune system from reaching the ganglion.

A

LATs (latency associated trancript)

54
Q

____ replicates to higher viral loads in blood, high rate of transmission from mother to child
-it progresses more rapidly
-originated from SIV four sperate transmissions to humans from chimpanzees or low land gorillas
-went through antigenic drift so now it can infect humans, it switched species

A

HIV-1

55
Q

___originated in the sooty mangabey monkeys

A

HIV-2

56
Q

HIV-1 is complicated to make a vaccine because of all the different types of ___

A

clades

57
Q

means that is slow progression

A

lentivirus

58
Q
  • ____is a retrovirus that establishes a chronic infection that slowly progresses to AIDS
    -HIV infects and replicate within cells of the immune system
    -activated CD4 T cells are the major source of HIV replication
  • there are several routes by which HIV is transmitted and establishes infection
    -HIV variants with tropism for different co-receptors play different roles in transmission and progression of disease
A

HIV

59
Q

what is HIV looking for?

A

T cells and macrophages. CD4 t cells looking for CCR5 receptor

60
Q

___target effector memory (TEM) and resident memory (TRM) CD4 T cells, dendritice cells and macrophages. ___ of HIV are thought to represent the major population of virus that establishes initial infection.
-wants CCR5

A

R5 variants

61
Q

HIV virions that bind the ___ chemokine receptor so called X4 variants) target naive and central memory (TCM) CD4 T cells. X4 variants of HIV emerge after initial infection

A

CXCR4

immuno (3 decks)

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