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1.2.3. Infection > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

1
Q

What tissue are APC pathogen sensors (PRRs) found in?

A

Skin (SALT), mucous membranes, lymphoid organs, blood circulation

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2
Q

How do APCs capture pathogens?

A

Phagocytosis, micropinocytosis

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3
Q

Where are APC pathogen sensors (PRRs) found on the cell?

A

Extracellular (bacteria), intracellular (viruses)

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4
Q

Dendritic and Langerhans (APCs) present Ag to?

A

Naïve T cells

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5
Q

Macrophages (APCs) present Ag to?

A

Effector T cells

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6
Q

B cells (APCs) present Ag to?

A

Effector T cells and naïve T cells

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7
Q

What are effector T cells?

A

includes helper, killer, regulatory, and potentially other T cell types

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8
Q

Briefly explain capture/processing/presentation of extracellular microbes

A

PAMPs on extracellular microbe bind PRRs, phagocytosis, processed and Ag presented on MHC II, which can bind CD4+ T cells

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9
Q

Briefly explain capture/processing/presentation of intracellular microbes

A

Intracellular microbe broken down, processed and Ag presented on MCH I, which can bind CD8+ T cells

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10
Q

What does MHC stand for?

A

Major histocompatibility complex

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11
Q

MHC that can bind CD8+ are class I, where are they found?

A

All nucleated cells

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12
Q

MHC that can bind CD4+ are class II, where are they found?

A

Dendritic cells, macrophages, B cells

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13
Q

MHC I are what genes?

A

HLA-A, HLA-B HLA-C

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14
Q

MHC II are what genes?

A

HLA-DR, HLA-DQ, HLA-DP

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15
Q

Outline the key features of MHC class I and II and the benefits that gives

A

Co-dominant expression = both parental genes expressed = increased number of diff MHC.

Polymorphic genes = diff alleles = increased presentation of diff Ag

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16
Q

Briefly outline the exogenous APCs pathway

A

Phagocytosis/micropinocytosis, matched to MCH II inside the cells, expressed on the surface of the cell, to a CD4+

17
Q

Briefly outline the endogenous pathway of Ag presentation in all cells

A

Virus or tumour Ag is broken down by proteasome to antigenic peptide, matched to MHC I inside ER then presented on the surface of the cell, to a CD8+

18
Q

What is the diff between slow and rapid processors in terms of HIV?

A

Slow = MHC present key peptides for survival of virus = effective T cell response. Rapid = MHC present mutated peptides = poor recognition and poor T cell response

19
Q

What are the downsides of MHC molecules?

A

Major cause for organ transport rejection, autoimmune disease when process is faulty

20
Q

When CD4+ T cells are activated what immune response takes place?

A

Humoral immunity = Ab, complement.

Cell-dependent immunity = Ab, complement, macrophages.

21
Q

When CD8+ T cells are activated what immune response takes place?

A

Activation of cytotoxic T cells

22
Q

Give examples of intracellular vs extracellular microbes

A

E = bacteria parasites, worms, fungi. I = viruses bacteria, protozoa.

23
Q

What is a T helper cell and its role?

A

CD4+ cell = assist other white blood cells in immunologic processes, including maturation of B cells into plasma cells and memory B cells, and activation of cytotoxic T cells and macrophages

24
Q

How are T helper cells defined?

A

secrete different cytokines to facilitate different types of immune responses = TH1, TH2, TH3, TH17, TH9, or TFH

25
Q

How is the right T helper cell activated?

A

First signal = naïve TH0 CD4 binds APC MHC II.

Second signal = naïve TH0 CD28 bind APC CD80/86 = co-stimulatory molecules.

Activated T helper cell releases:

IL-2, autocrine, actives proliferation = TH1 for intracellular microbes,

OR

IL-4 switches to TH2 or TH17 for extracellular microbes

26
Q

Outline the T cell response to intracellular microbes

A

Activated by binding APC:

TH1 CD4+ prod IFN-γ which causes B cells to switch to plasma cells and macrophages to become active both killing opsonised microbes.

TH1 CD4+ also activates CD8+ (which will bind MHC I)

27
Q

How do CD8+ cells kill?

A

Bind MHC I = prod perforin (makes holes) and granzymes (starts apoptosis)

28
Q

Outline the T cell response to extracellular microbes

A

TH17 CD4+ bind APC = IL-17 prod = neutrophils activated = phagocytosis.

TH2 CD4+ bind APC = Il-5 = activates eosinophils, IL-4 = activated B cells + mast cells

29
Q

How does B cell Ab/Ig production differ in primary vs secondary responses?

A

P = high IgM. S = High IgG

30
Q

Name each Ig and where it is found

A

IgG = secondary response, complement neonatal immunity. IgE = allergies, helminths. IgA = mucosal. IgM = primary response, complement

31
Q

What happens if there are no CD4+ cells e.g. HIV?

A

there is no activation of CD8+ T cells

32
Q

What is cross presentation?

A

feature of APC

can present intracellular microbes on MHC I and II to activate both CD4+ and CD8+

1.2.3. Infection (13 decks)

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