Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microimm 2500 > (I) Lecture 7: T cell Immunity Part II > Flashcards

(I) Lecture 7: T cell Immunity Part II Flashcards

1
Q

Where do lymphocytes develop?

A

B cells develop in the bone marrow

T cells start in the bone marrow then finish developing in the thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are lymphocytes activated and differentiated?

A

In the secondary lymphoid tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adaptive immunity specificity

A

B and T cells express many exact copies of a receptor w/ a unique antigen binding site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

T cell receptors

A

Each T cell has a TCR with a variable region specific for one unique peptide even if there are multiple TCRs on a T cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Types of effector T cells

A

Helper cells (CD4+) = exogenous (MHC Class II)
Cytotoxic T cells (CD8+) = endogenous (Class I)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cytosolic pathogens

A
  • degraded in cytosol
  • peptides bind to MHC Class I
  • presented to CD8 (cytotoxic) T cells = cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Intravesicular pathogens

A
  • degraded in endocytic vesicles (low pH)
  • peptides bind to MHC Class II
  • presented to CD4 (helper) T cells = activation of macrophages to kill intravesicular bacteria and parasites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T cell differentiation

A
  1. antigen recognition
  2. activation
  3. clonal expansion
  4. differentiation
    - effector functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CD4 function

A

activation of macrophages, B cells and other cells

Recognize complex of bacterial peptide w/ MHC Class II and activates macrophage
- help macrophage phagocytose better (induce fusion of phagolysosome or improve outcome of phagocytosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

CD8 function

A

killing infected “target cells” AND macrophage activation

Recognizes complex of viral peptide w/ MHC class I and kills infected cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T cell activation

A

Thymus –> SLT –> site of infection

naive T cells enter SLT looking for their respective antigens/pathogens (activated by DC)

effector T cells are activated then leave SLT and enter infected tissue (innate signaling) to either kill (CTL) or “help” (Th) control the infection – proliferate and eliminate infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

SLT

A

Secondary Lymphoid Tissue

SLT (lymph nodes, spleen, MALT) are specialized to facilitate interaction of circulating T and B lymphocytes with their antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lymph node and T cell activation

A

Antigen comes in lymph (either free antigen or bound to DC)

In T cell zones, naive T cells can recognize antigen on the surface of DC

Effector T cells leave lymph node to travel to infected tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Antigen Presenting Cells

A
  • INITIATE adaptive response
  • presents pathogens: expresses antigens of pathogens on their surface on MHC I or II
  • migrate to SLT and to T cell zones
  • ONLY DCs can activate naive T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are naive T cells activated?

A

Through MATURE dendritic cells (DCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ways that an APC can engulf antigens

A
  1. Phagocytosis through a phagolysosome
  2. Pinocytosis: macrophages and DCs engulf fluid by protruding actin filaments (endosome)
  3. Endocytosis: B cells can use endosomes to engulf pathogens

Result in loading of antigenic peptides onto MHC Class II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Dendritic cells roles (maturation)

A

Immature DC: phagocyte (innate immunity)
Mature DC: antigen presentation (adaptive immunity)

18
Q

Dendritic cell maturation steps

A

DCs mature after they travel in lymphatic tissue

  1. immature DCs live in peripheral tissues
  2. DCs migrate via lymphatic vessels to lymph nodes
  3. Mature DCs activate naive T cells in lymphoid organs like lymph nodes
19
Q

DCs and receptor-mediated phagocytosis

A
  • Pathogen presented: extracellular bacteria, fungi
  • Presented to: MHC Class II
  • Activates CD4 T cells
20
Q

DCs and macropinocytosis

A
  • Pathogens presented: extracellular bacteria, soluble antigens, virus particles
  • Presented to: MHC Class II
  • Activates CD4 cells
21
Q

DCs and viral infections

A
  • Pathogens presented: viruses (ENDOGENOUS)
  • Presented to: MHC Class I
  • Activates CD8 cells
22
Q

DCs in SLT

A
  • antigen presentation
  • trigger clonal expansion and differentiation
  • CD4+ gives rise to T helper cells
  • CD8+ gives rise to cytotoxic T cells
23
Q

Constant activation of T cells

A

Can lead to severe outcomes like superantigens

24
Q

Signals of T cell activation

A
  1. TCR binding to antigen/MHC
  2. Costimulatory receptors (expressed only by APCs)
  3. Cytokines (secreted by APCs)

ALL three must be present for full activation and clonal expansion

25
Q

T cell anergy

A

Lack of costimulatory receptor (non-APC cell) fails to activate T cell
- good b/c you don’t want T cells attacking good cells

Anergic T cell continues through circulation w/o activity

Good CHECKPOINT: stops autoreactive T cells

26
Q

How do CTL cells kill infected cells?

A

They kill cells infected w/ intracellular pathogens like viruses via induced cell-mediated APOPTOSIS

CTLs have granules loaded w/ toxic stuff that migrate to site of infection and releases substances (like w/ NKCs)

27
Q

Perforin

A

In CTL granules

  • form pores in membrane of target cells
  • helps in delivering contents of granules into cytoplasm of target cell
28
Q

Granzymes

A

In CTL granules

  • degrades DNA of target cell = triggers APOPTOSIS
29
Q

CTL steps

A
  1. motile mouse CTL approaches target cell
  2. initial contact
  3. start of exocytosis (granules fuse w/ CTL cell membrane and perforin is released)
  4. granules congregate to CTL/TC (target cell) contact
  5. more granules migrate
  6. granzyme starts a cascade of rxns that fragment target cell DNA = APOPTOSIS
    - viral RNA is also degraded
30
Q

Viral infection course of response

A
  1. Virus infected cells release IFNs
  2. IFN stimulates NK cells which kill virus-infected cells and help control infection WHILE CTLs generate
  3. CTL continues to kill virus-infected cells = infection is controlled
31
Q

T helper cell response

A

T helper cells regulate immunity to intravesicular pathogens

Secrete IFN-gamma which enhances phagocytosis

T helper cells also form a granuloma if intracellular pathogen can’t be completely cleared

32
Q

IFNs

A

IFN alpha and beta activate NKCs
IFN gamma enhances phagocytosis (from TH1)

33
Q

Granuloma

A

A BARRICADE around infected macrophages if intracellular pathogens can’t be completely cleared

34
Q

SCID

A

Severe Combined ImmunoDeficiency

ABSENCE of functional T cells
- severe medical emergency = fatal w/o treatment
- no T cells = no activation of B cells (combined)
- infants w/ SCID die quickly from infections w/ opportunistic pathogens

  • newborn screening = early treatment
  • preventative treatment = prophylactic antibiotics + IVIG
  • Cure: hematopoietic cell (bone marrow) transplant
35
Q

AIDS

A

Acquired Immune Deficiency Syndrome

  • associated w/ Human Immunodeficiency Virus (HIV)
  • contact w/ virus does not necessarily mean infection
  • infection rate depends on route of contact (blood contact is highest)
  • no cure or vaccine yet

Treatment: antiretroviral therapy

36
Q

CD4 cells and HIV

A

CD4 is a receptor for HIV and binds to constantly activate T cells to point of T cell exhaustion = DECREASE in number of T cells

Frequent opportunistic pathogens = death

37
Q

Seroconversion

A

anti-HIV antibodies

38
Q

An effector T helper cell response is likely to result in

A
  • formation of a granuloma (for TB)
  • production of IFN-gamma (activates macrophages)
39
Q

Apoptosis

A
  • occurs at end of a cell’s lifespan (natural)
  • can be triggered by granzyme
  • kills infected cells
40
Q

What can contribute to elimination of intracellular virus?

A
  • MHC I molecules (endogenous peptides)
  • CTL
  • NK cells
  • Type I IFN (activates NKCs)

Microimm 2500 (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions