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BIIC > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the role of the Major Histocompatibility Complex (MHC)?

A

Present portion of antigens to other cells.

Lock and key for each pathogen.

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2
Q

What do NK cells do to those who don’t have MHC class 1?

A

Kill them without discrimination.

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3
Q

What are B cell epitomes?

T cell?

A

Surface piece of antigen or secreted molecule/toxin to which the antibody binds. Usually conformational.

T cell epitomes are small processed pieces of antigens that must be linear!

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4
Q

What are the differences between Class 1 and 2 MHC?

A

Type one expressed on most nucleases cells and is recognized by CD8 T cells

Type 2 expressed on professional APCs and is recognized on CD4 T helper and CD8 T cells

These have to deal with histocompatibility due to the recognition of Class 1 or 2 in organ receivers.

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5
Q

Explain Dendritic Cell Migration to nearest lymph nodes

A

Inflammatory signals at site of infection (IL-1, IL-6, TNF-a Major inflammatory marker)

Lose adhesiveness for epithelia. Express CCR7 (chemokine receptor 7) a concentration gradient from lymph node (where the concentration is highest) that the cell can follow to the infected node.

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6
Q

Which is more in the middle the B zone or T zone in the lymph node?

A

T zone. B zone is around that middle T zone.

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7
Q

What is the structural difference between MHC class 1 and 2?

A

Class one is a B2-microglobulin that makes up the whole cleft.

Class two has two strands that make up the binding cleft.

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8
Q

Explain the Antigen Binding cleft and what is needed to activate T cells?

A

MHC does not have fine specificity.

Takes about 100 MHC interactions to activate T-cells.

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9
Q

What is an Anchor residue?

A

It is the small portion of the peptide at the bottom that bind to the MHC class 1.

The peptide fits in the MHC like a ball in a glove. Large space with small peptide. The anchor residue is what keeps the peptide in.

The residues are more hydrophilic. The hydrophilic area bulges out and is what comes into contact with the T-cell.

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10
Q

Describe the cleft of MHC type 2?

A

Longer peptides of 10-30 AA

Cleft is open at both ends and so the peptide is coming out both sides like a hotdog in a bun.

Internal Conserved Motifs are what bind instead of anchor residues.***

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11
Q

Which class is best at fighting extracellular bugs vs intracellular bugs?

A

MHC class 2 is better at extracellular pathogens. Via B-cells and cytokines

MHC class 1 is for intracellular via CD8 and cytotoxic T-cells.

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12
Q

What is the MHC class 1 cytotoxic pathway/Endogenous (intracellular antigens)

A
  1. Protein gets ubiquitinated
  2. Proteosomes chop up proteins into peptides
  3. TAP (Transporter Associated w/ antigen Processing) uses ATP to translocation peptides into ER lumen
  4. Tapasin links empty Class 1 to TAP for easy access to incoming peptide (by chaperones)
  5. Peptide fitting into binding cleft releases chaperones
  6. Stable MHC - Transported to surface
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13
Q

What is the MHC class 2 Exogenous/Endocytic Pathway (Extracellular antigens)

A
  1. Constantly, MHC class 2 are synthesized and assembled in the ER. The a and B are held together by chaperones with invariant chain*** (holds the presenter open)
  2. MHC class 2 is transported through the Golgi to MHC class 2 compartment
  3. Extracellular protein gets taken up by APC into endosomes
  4. Proteins become target of poteasomes
  5. Proteosomes chop up the antigenic proteins in endosomes that fuse with MHC Class 2 Compartment.
  6. Enzyme digest chain leaving only CLIP (Class 2 invariant chain peptide.
  7. CLIP is replaced by HLA-DM chaperone to put antigenic peptide
  8. Stable MHC 2 is transported to surface.
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14
Q

What do Inhibited proteosomes lead to and why is it relevant?

A

Apoptosis

Important for cancer to induce apoptosis in specific tumor cells.

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15
Q

What is Cross Presentation?

A

Special Case

When a peptide derived from extracellular environments get redirected to the cytosolic pathway for presentation by MHC class 1.

Dendritic cells are best at this. This helps get CD4 and CD8 responses.

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16
Q

Describe MHC Nomenclature

A

HLA: Human Leukocyte Antigen

Class 1- HLA-A, B, C
Class 2- DQ, DR, DP

Having different MHCs makes a person less likely to get a certain disease.

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17
Q

Why is chromosome 6 important?

A

Codominat expression and extremely polymorphic for MHC.

Father and Mother give a combination of their MHC to their kids so even the kids don’t have the same.

FAMILY MEMBERS HAVE DIFFERENT HAPLOTYPES FROM PARENTS

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18
Q

What are TCR?

A

They are receptors that T-cells use to interact with MHC on other cells.

Only binds to the MHC with the peptide.

TCR has gamma delta T-cells that do recognize free or processed antigens.

The common TCR is alpha beta which was already explained.

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19
Q

What are cellular clones?

A

They are T-cells that all have the same specificity to a certain antigen.

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20
Q

What are the stages of T cell maturation?

A

Pro T-cell: Proliferating and recombination of B chain

Pre-T cell: Rcombination of the a chain

Immature T-cell: Have TCR but express both CD4 and CD8 (double positive)

Mature T-cell: Downregulates either CD4 or CD8 to become a single positive.

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21
Q

What is the Goldilocks Principle?

A

Positive selection that has weak recognition of MHC presenting self-peptide

Negative selection too strong or no recognition of self-peptide within MHC results in apoptosis.

Not too hot and not too cold. Just right.

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22
Q

On the T-cell synapse what is in charge of signal transduction and what is in charge of stabilizing or adhesion?

A

Signal: CD3, and ITAM

  • Also CD28 in costimulation activating signal that binds to B7
  • CTLA-4 and PD-1 Inhibit the T-cell expression binding to B7 and PD-1

Stabilize and adhesion: CD4 or CD8
-Also LFA-1*** not important

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23
Q

What would antibodies binding to CTLA-4 do?

A

Stops inhibition of T-cells and continues activation.

Used to treat Melanoma. Changes the T-cells from tolerating the cancer to acting against it.

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24
Q

How can bacteria take advantage of the Immunological Synapse (IS)

A

They stay near the junction point and jump to the T-cell when the synapse is occurring.

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25
Q

What signals the proliferation event during the synapse?

What is produced if T-cell is activated?

A

IL-2 induces T-cell proliferation******* HAS TO HAPPEN

  1. Signal is antigen recognition by MHC/TCR
  2. Signal is C28/B7 costimulation.

One of three things is produced:

  1. NFAT
  2. NF-kB
  3. AP-1
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26
Q

Explain CAR T-cell Therapy

A

T-cell is taken and adjusted to fight cancer.

IL-2 is added to proliferate cell into millions of T-cells.

Those cells are reintroduced into the body.

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27
Q

How does IL-2 bind to T-cells

A

Uses and autocrine pathway and a JAK/STAT receptor to begin proliferation.

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28
Q

What drugs target NFAT to stop IL-2?

When are they used.

A

Cyclosporine
Tacrolimus

Used for bad RA, Psoriasis and Organ Transplants

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29
Q

After proliferation of the T-cell there is further differentiation.

What can T-cells become?

A

Effector T-cells (short lived) helper and cytotoxic that are primary immune responses

Memory T-cells: (Long lived). Respond to any subsequent infections.

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30
Q

What stops T-cell Proliferation

A

After several round the T-cell expresses CTLA-4 and that binds to B7 to inhibit proliferation.

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31
Q

What are the types of Effector Helper T cells

A

TH1 cells cell mediated reactions
(Bacteria, virus, fungi, chronic inflammation) Intracellular

TH2 Humoral reactions
(Parasites and allergens) Extraceullar

TH17 inflammatory disorders and some microbial defense
(Extracellular pathogens and autoimmune disorders)

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32
Q

What environment leads to the activation to the 3 kinds of T-cells?

Where do the cytokines in the environment come from?

A

IL-12 and IFNy to TH1
(Made by Dendritic and NK cells)

IL-4 to TH2
(Made by own T-cell)

IL-6 and TGF-B to TH17
(Released by lots of different cells at mucosal surfaces)

From Macrophages and Dendritic cells generally

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33
Q

What is the primary function of TH1 cells?

What cytokines do they excrete?

A

Activate and support phagocyte mediated defense against intracellular infections

IFN-y
IL-2
TNF-a
(CD40L/CD40)

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34
Q

What is the primary function of TH2 cells?

Which cytokines do they excrete?

A

Stimulate B cells to produce antibodies and in eosinophil/mast cell mediated reactions in response to extracellular antigens.

IL-4, 5, 13

Regulates humoral functions

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35
Q

How do TH2 cells help with healing?

A

They signal M2 macrophages to help with healing.

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36
Q

What is the primary role of TH17 cells?

Which cytokines do they secrete?

A

Response to extracellular pathogens. They are prevalent in inflammatory conditions (including autoimmunities)

IL-17, 21 (self-acting), and 22

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37
Q

Explain the function of CTL cells

A

Effector Cytotoxic T Cells (CTLs)

They kill using cell-to-cell contact.

They have 3 mechanisms of killing using Granzymes/Perforin, Fas, and Cytotoxic Cytokines - TNF.

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38
Q

Explain Perforin and Granzymes

A

Perforin makes the hole in the cells, and then Granzymes are let in to cause apoptosis

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39
Q

Explain Fas-FasL mechanism?

A

CTLs use Fas receptors on all of our cells. CD8 T-cells (CTLs) are the only cells that express FasL.

The interaction of Fas and FasL triggers apoptosis.

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40
Q

Explain how CTLs use cytokines to induce cell death

A

A very concentrated package of TNF-a will induce apoptosis across the immunological synapse

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41
Q

Explain the function of Superantigens

A

Superantigens can connect any MHC to any TCR whether it be a CD8 or CD4 T-cells.

They can cause massive amounts of cytokines or unregulated cell death from CD8 cells.

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42
Q

Explain Scalded Skin Syndrome and what is its cause?

A

Staph Aureous
Bullard

Using 2 Superantigens (Epidemolytic toxins A and B)

Present in children under 5.

Lots of blisters, and red skin. Will have positive Nikolsky’s sign (top layer of skin detaches with gentle rub)

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43
Q

Explain a Cell Mediated Immune (CMI) Response to intracellular Bacteria

A

Macrophage with intracellular bacteria makes IL-12 which activates NK cells.

NK cells make IFN-y to make Macrophage a better killer and superactivates the NK cell to kill better.

Connection with CD4 TH1 cells will also help express CD40 on the macrophage and CD40L on the CD4 cell to make the macrophage even more ROS to kill bacteria.

44
Q

What happens if after IFN-y and CD40 the macrophage can’t kill the bacteria inside of it?

A

Macrophage will display antigen on Class 1 MHC and CD8 T-cells will kill the cell.

45
Q

What is the first line of defense against CMI Response to Viruses?

What else is made to fight viruses?

A

IFN-a and IFN-B to activate NK cells to destroy Viruses

These Interferons also activate antiviral mechanisms, increase class 1 MHC and stimulate more NK cells

RNAse is also made and translation is slowed down.

46
Q

Which cells do NK cells target?

A

Cells that have downregulated MHC 1.

47
Q

Explain what Memory T cells do and how they are different than effector cells?

A

They persist for years and even a lifetime after CMI response to a pathogen. Uses IL-7 receptors to stay viable.

The secondary immune response is much more rapid and amplified.

48
Q

Explain T-cell exhaustion

A

T-cells are sprinters. They proliferate destroy and then leave.

Chronic infections stay long enough that they can exhaust the T-cells to the point where they can’t fight the infection all the way off.

49
Q

Explain Regulatory T-cells and how they are different from other T-cells

A

They are CD4 positive, but aren’t helpers. They also have FoxP3.

They down-regulate the immune response. And inhibit the auto-reactive T-cells

They do this by expressing lots of CTLA4 and secreting antiinflammatories
-IL-10
-TGF-B
They also have lots of IL-2 receptors to outcompete other effector T-cells.

50
Q

IPEX Syndrome

A

Immunedysregulation Polyendocrinopathy Enteropathy X-linked

Defect in FoxP3

Severe autoimmunity.

Early onset severe diarrhea, Type 1 diabetes, severe derm problems

Classic Triad of: Enteropathy, endocrinopathy, and dermatitis

51
Q

What is Allogeneic?

A

It is having the same dissimilar genes.

Isogeneic is the same genes.

52
Q

What is H blood?

A

You can’t receive A, B, or O blood. You have to receive H blood.

53
Q

When is the Rhesus factor a problem?

A

When father is Rh+ and mother is Rh- The mother will make antibodies to the + Rh. On the next child, if they have + the mother will attack.

Hemolytic disease of the fetus or newborn HDFN. Complement forms MAC to kill RBC

54
Q

Whole Blood?

A

Shelf life 35 days

Collected In anti-coagulant

Indication: Trauma and massive blood loss

High military use

55
Q

RBC transfusion

A

Preserves up to 42 days.

Indication: Correction of defect in oxygen-carrying capacity, chronic anemia’s

Type O RBCs are used in patients with unknown blood type in emergent situations.

56
Q

Leukocyte-reduced RBCs

A

WBCs are removed in LRRC

Indications: Prevent febrile nonhemolytic transfusion reaction.

Prevent TRIM (Transfusion-Related Immunomodulation).

57
Q

Washed or Irradiated RBCs

A

Washed
Removal of plasma proteins

Indication: Patient has had an allergic transfusion reaction.
-Also use in IgA deficient patients. Exposure to IgA blood can lead to anaphylaxis.

Irradiated RBC

Indication: Prevention of rare but often fatal transfusion-associated GVHD in immuno-incompetent recipients.

-Patients with blood cancers, Neonates, stem cell transplant recipients.

58
Q

Frozen RBC

A

Freezing destroys most blood constituents other than RBC and small amount of WBC

Frozen storage up to 10 years. Must use within 24 h after thawing

Stockpile of rare donor types
Use in Autologous donations for later use. Has high cost.

59
Q

List some transfusion reactions

A

Febrile nonhemolytic transfusions: pretty common
-fever, chills, rigors

Acute Hemolytic: Blood is being lysed.
-fever chills vomiting, hypotension, tachycardia, back pain.

Hypervolemic
-Dyspnea, tachycardia, HTN, headache, jugular venous dissension
ABO-incompatible blood transfusions.

Transfusion-related acute lung injury

60
Q

Acute Intravascular Hemolytic Transfusion Reaction

A

Complement proteins— massive inflammatory event.

MAC: Hemolysis gives hemoglobinemia, and hemoglobinuria (red/dark urine)

Cytokines
-Inflammatory: IL-1, IL-6, and TNF-a
—Fever, renal vasoconstriction

IL-8: Neutrophil chemotaxis and activation. Blood pressure drops, and tissue edema

Treatment: Stop diffusion watch for bad reactions as it can be fatal.

61
Q

Delayed Hemolytic Transfusion Reactions

A

3-10 days post-transfusion

Presentation less emergent than acute. Fever, falling hematocrit.

Renal monitoring.

Is more serious in sickle cell patients. Usually happens for people who have had previous transfusion.

62
Q

Acute Extravascular Hemolytic Transfusion Reactions

A

Clinical signs: Fever/chills, jaundice, clinically stable

Labs: increased bilirubin, increase LDH

Usually happens from an incompatibility in another blood protein.

63
Q

Febrile Nonhemolytic Transfusion Reactions

A

Fever, chills, rigors

Rise of 1 deg C or over 38 deg C during transfusion with no other reason for fever.

Due to build up of cytokines in donor unit.

LRRCs prevent this reaction (Leukocyte reduced RBC)

64
Q

TRALI

A

Transfusion Related Acute Lung Injury

Within 6 hrs of start of transfusion

Signs and Symptoms: Hypoxemia, fever, hypotension, tachypnea, pulmonary edema

Pathogenesis: HLA/granulocytes-specific antibodies (from donor).reacts with endothelium of lungs.

Diagnosis: Radiograph, blood gases.

Initial Diagnosis often fluid overload, anaphylaxis

Treatment: Stop transfusion, provide respiratory support. May need intubation

65
Q

Transfusion-Transmitted Diseases

A

Serration Marcescens- Gram-negative bacillus Red at room temp

Staph aureus

Staphylococcus epidermidis

E. Coli- gram-negative bacillus

Strep species (gram Positive)

66
Q

Nucleic Acid Amplification Testing

What else can help reduce pathogens in blood transfusions?

A

MP-NAT — minipool NAT

Basically PCR to keep infection out of blood samples

Filters, UV Light and culturing Tech
-Blood cell substitutes (perfluorocarbons, hemoglobin-based O2 carriers, Stem cell derived)

67
Q

What are the B-cell receptors?

A

Membrane-bound antibodies

68
Q

What is the selection process of B-cells?

A
  1. Failure to express preantigen receptor
  2. Needs to express one chain of the antigen receptor
  3. Needs to express the complete antigen receptor.
  4. Need to have weak antigen recognition
69
Q

Where do B-cells mature

A

Bone marrow in Hematopoietic marrow.

70
Q

Bruton Agammaglobulinemia

A

X-linked recessive

Mutation in Bruton’s tyrosine kinase which is essential for BCR signaling.

No visible tonsils.

Unusual infections early in childhood.

Very low or absent antibodies anywhere.

Treatment: Give purified antibodies. Bone marrow transplant, but that is very dangerous because of lack of antibodies.

71
Q

How are diverse antibodies created?

A

Variable regions using RAG, which is recombination activating gene.

Heavy chain moves first, and then the light chain.

V, D, and J

72
Q

What are the steps of B cell gene rearrangements?

A

Early Pro-B-cell
-H-chain gene rearrangement

Late pro-B cell
- H-chain gene rearrangement

Pre-B cell
- L-chain gene rearrangement

Immature B cell
-Rearrangement ceases.

Cell is expressed.

73
Q

What is Anergy

A

Unresponsive B cells. They have weaker reaction to self antigens and can’t respond to subsequent antigen encounters

We don’t know whey they are released.

74
Q

What is the Receptor Editing

A

B cell that react strongly with self antigens can undergo clonal deletion or receptor editing before they are apoptosed.

Different from T-cells

75
Q

What is B-cell Clonal Ignorance

A

B-cells that are self-reactive, but do not respond during development become clonally ignorant.

After disease, these cells become activated and can lead to autoimmune diseases.

These cells are not anergic

76
Q

What is the final step of B-cells maturation?

A

B cells have IgM and then migrate to the periphery to make it to the spleen.

The spleen has a survival signal that adds IgD to the surface fo the B-cell.

It also gets CD19, CD20 are particular to B-cells

CD21 (from the spleen) for survival

77
Q

What are Marginal Zone B cells?

A

B-cells that stay in the spleen. They help recognize blood born pathogens.

These don’t have IgD. Only circulating B-cells have IgD

78
Q

What is Affinity Maturation

A

After an isotope switch from IgM to IgG, those IgG get better at binding to their antigens. They become more high affinity to those cells.

79
Q

Describe B cell activation

A

Main job of B-cell is secreting antibodies.

IgM is first to be secreted.

Cytokines form Helper T-cells, macrophages, or other B-cells, induce isotope switching to other antibodies, but it takes time

80
Q

What are the two ways that B-cells become activated?

A 
With T-cell help:  more affinity maturation, induction of memory, better class switching.
(Thymus Dependent)
Without T-cell help:  Less memory, affinity, and class switching.  They come from Marginal Zone B-cells that respond to non-protein antigens
(Thymus-independent)
81
Q

What is the signaling to activate B-cells?

A

First signal: antigen binds to Membrane-bound antibody

  1. Crosslinked BCR’s. Antigen binds to 2 close antibodies.
  2. Signal sent by Iga and IgB to activate Transcription factors.
  3. Cell proliferation and differentiation.

Second signal: engagement with helper T cell using CD40 and CD40L (from T cell)

82
Q

What happens after Signal one crosslinking in B-cells

A

Consequences of crosslink signal:

  • More MHC class 2 expression (to keep only helper T-cell. For extracellular antigens)
  • B7 expression increases
  • Internalization of antibody: antigen complex
  • Activation of adhesion molecules
  • Expression of CCR7
  • Migrate to edge of follicle to interact with Tcells

Proliferates, recruits T-cells, migrates from follicle, secretes antibody

83
Q

Describe just Signal 2 for B-cells

A

Used for T-Dependent Antigens

MHC:TCR + CD40:CD40L

84
Q

Explain Indirect damage and Direct Damage to the host

A

Indirect: Damage by immune system:

  • Immune complexes: glob of Ab and pathogens
  • Anti-host antibody: Hemolytic anemia
  • Cell Mediated immunity

Direct: Damage by pathogen

  • Exotoxins Production
  • Endotoxins
  • Direct cytopathic effect
85
Q

What is an extracellular Bacteria?

A

Bacteria that replicate outside the host cells

86
Q

What is the #1 cause of death in ICUs?

Which bacteria causes it?

A

Septic Shock

Gram negative bacteria expressing LPS activate macrophages in the spleen and liver

Bacteremia leads to septicemia (have the bacteria and the toxins) that produces an inflammatory response

87
Q

What is Toxic Shock?

A

Extracellular Bacteria

Inflammation mediated tissue destruction.

Exotoxins, enterotoxin, and endotoxins.

88
Q

What leads to fever and what does it regulate?

A

Endogenous Pyrogens

From the hypothalamus.

89
Q

How do Macrophages and NK cells work together

A

Intracellular bacteria that can’t be broken down by macrophages cause the release of IL-12. That activates NK cells who will secrete IFN-y to add more ROS.

TH1 cells are also activated by IL-12 and they make even more IFN-y.

90
Q

What is Valley fever?

A

Caused by fungi and TB in the dirt that cause granulomas within the lungs or elsewhere.

As we age, and the immune system wanes, those granulomas break, and you get a reoccurrence of valley fever or TB.

91
Q

What is a granuloma?

A

Epithelial cells (large macrophages) multinucleated giant cells, and fibroblasts with T cells that wall-off the pathogen that can’t be killed.

92
Q

What are Defensins

A

A short peptide that is hydrophobic.

They jump into fungi, and bacterial cell walls and cause holes to form. Self-cells have peptides that break defensins.

93
Q

What is Farmer’s Lung

A

Hypersensitivity pneumonitis

Immune-complex mediated from an allergen. An allergy to inhaled mold (mostly straw or grain)

94
Q

Explain the 2nd signal of b-cells for T-independent antigens

A

Don’t need the MHC-TCR or CD40-CD40L step

Need a non-protein antigen in Marginal zone or from B-1 cells. They make IgM but they responses are short and don’t generate memory

95
Q

What is transient hypogammaglobulinemia of infancy?

A

From 6 m to 24 m.

Recurrent infant infections due to unprotection by maternal antibodies.

96
Q

What do B-cells do in Germinal centers

A

Proliferate
Affinity maturation
Isotope Switching

97
Q

Which cytokines will cause Isotype (class) switching of the heavy chain of the Ab of B-cells?

A

IL-4, TGF-B, IFN-yto IgG

IL-4 to IgE

TGF-B to IgA (stop gut inflammation)

Specificity doesn’t change

98
Q

What are plasma cells?

Memory Cells?

A

Short lived activated B-cells that just pump out antibody.

They are generated from cells that have undergone affinity maturation

99
Q

What is the most common primary immunodeficiency?

A

IgA deficiency,

90% asymptomatic

Will get recurrent GI and URI.

Transfusions may be tough because you could have anti-IgA reactions.

100
Q

What is Hyper IgM

A

X-linked

Decreased presence of other isotypes they are just making IgM

101
Q

What is common variable immunodeficiency

A

Low levels of IgG, IgA, and IgM.

Usually diagnosed after someone gets a vaccine for a bug, and then gets that infection.

High susceptibility to chronic lung disease

102
Q

What is tolerance?

A

A state of unresponsiveness by lymphocytes

Central and peripheral

103
Q

How do we lose self tolerance?

A

Failure of central tolerance in primary lympoid tissue (negative selections)

Failure of peripheral tolerance in secondary lymphoid tissue.
(T or B cells become anergic, are suppressed, or are deleted via apoptosis)

104
Q

What is AIRE?

A

Self antigens in the Thymus to make sure that T-cells won’t leave and attack

105
Q

Where is there immune privilege? What is it

A

Places where there aren’t immune responses

Brain, Eye, uterus, Testis

More Tregs and Reduced MHC

106
Q

When will we see failures of tolerance?

A

We use T-reg, and macrophages to keep our own immune system in check

Mutations in immune genes, MHC alleles, Infections with molecular mimicry will produce a failure of tolerance

107
Q

What is Molecular Mimicry

A

A way that infection can stop tolerance. Microbial epitomes that are similar to those from self-antigens can then activate T and B cells against self

  • cross-reactive T cells
  • cross-reactive antibodies

BIIC (8 decks)

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