Immunology Exam 2

MHC class I presents _____ peptides to _____, whereas MHC class II presents _____ peptides to _____.

endogenous, CD8+ T cells; exogenous, CD4+ helper T cells

Know the steps of T cell development in order.

1) T-cell precursors exit the bone marrow and traffic to the thymus

2) T-cell precursors travel to the outer thymic cortex where they proliferate

3) T cells begin to express their T-cell receptors

4) T cells undergo positive and negative selection

5) Mature T cells migrate to the thymic medulla before exiting the thymus

Know characteristics of gammadelta T cells.

First to arise during fetal development

Decline after birth

Common in tissues

Recognize unconventional antigens

Lipids, stress ligands, etc.

DO NOT exit thymus with ability to kill

What is clonal anergy?

A state of nonresponsiveness that helps to provide self-tolerance

What are APCs? Give examples.

• Antigen presenting cells -> they alert adaptive immune system of a threat by expressing MHC 2

• Dendritic cells

• Macrophages

• b-cells

not t-cells

What do strep pyrogenic exotoxins do? Why do physicians usually treat a positive streptococcal test in the presence of sore throat with antibiotics without hesitation?

• Exotoxins cause rheumatic fever and shock

  Cross-link MHC II to the TCR outside the peptide groove, causing polyclonal T cell activation

  Then a cytokine storm leading to fever, toxic shock syndrome, and scarlet fever

  
  

What interleukin do stromal cells use to support B cells?

IL-7 (made by stromal cells in bone marrow to help develop B cells)

Stimulates progenitor cell survival, proliferation, and transcription

NOT IL-2 (survival and proliferation in T cell and B cell)

Put steps of B cell development in order.

1. STAGES: Pre pro B→ Early pro B → Late pro B→ Large pre B→Small pre B→ Immature B

   STEPS: HSC →CLP →pro-B: heavy chain D-J then V-DJ rearrangement

   Pre-B: mu heavy chain + surrogate light chain = pre-BCR; light chain rearranges

   Immature B: surface IgM; central tolerance test

   Transitional B → leaves marrow

   Mature naive B

   
   

What happens if a BCR tests positive for reaction with self?

• Receptor editing (rearrange light chain_

• If that fails, apoptosis

What 2 things need to be transplanted for a lethally irradiated mouse to produce antibodies?

1. Bone marrow

2. Thymus transplants (antibodies)

What cells support long-lived plasma cells in the bone marrow?

Bone marrow stromal cells

Know functions of antibody isotypes.

• IgM: first antibody produced in a primary response; pentavalent (not produced by mB cells)

  IgD: naive B cell surface receptor with IgM; promotes basophil and mast cell release of AMPs

  IgG: includes several subclasses, some of which are particularly good at complement fixation

  IgA: found in secretions; effective at neutralizing toxins and pathogens

  IgE: best known for roles in allergy, asthma, and parasitic worm infection

  
  

Know what perforin and FAS-FASL interactions do.

• Forms pores in the target membrane so granzymes enter

• Leads to caspase activation then apoptosis (mediator)

What do NK cells detect that CTLs don’t?

NK detects lack of MHC class I

CD8+ detects antigen in MHC class I receptors

What are the adaptive effector cells of cell-mediated immunity?

CD8+ CDLs (Tc cells)

CD4+ T helper subsets

What are the innate and adaptive cytotoxic effector cells?

Innate: NK cells

Adaptive: CTLs

What are effector functions of complement fixation?

Opsonization, inflammation/chemotaxis, lysis, immune complex clearance

What is the first antibody isotype produced in an immune response?

igM

What does IgA do for mucosal surfaces?

Neutralizes pathogens/toxins and blocks their attachments

Controls commensal populations

Forms dimer at mucosal surfaces

Which Fc receptor interacts with IgE (if you know Greek letters this is a gimme question)?

Epsilon ε

Know steps of CTL activation and function.

APC presentation to Th+CTL (cytotoxic lymphocyte)(helper cell)

Allows for activation of cell and circulates in activation state

Infected cell presents antigen in MHC class I

Immunological synapse formation

Perforin and granzymes are released (apoptosis) (FAS+FASL ligand interactions)

Does NOT involve histamine because it is different all together (MOST LIKELY GONNA INVOLVE THIS)

Know what cell could detect an intracellular infection inhibiting display of MHCs.

NK cells

What do celiac disease and ulcerative colitis have in common?

are inflammatory diseases that occur in the gut.

What does it mean that gut cells are “polarized”?

distinct apical and basolateral surfaces

Where are Peyer’s patches and isolated lymphoid follicles?

• GALT

• Peyer's patches: small intestine (mainly ileum)

• Isolated lymphoid follicles: throughout the small and large intestine

What cell layer is found in the respiratory tract, not the GI?

a mucociliary layer

What cells compose a dead outer protective layer in the skin?

Keratinocytes --> corneocytes

AID converts cytosine into ______________.

Deoxyoridine (results in change in code when it gets repaired)

Where do long-lived plasma cells stay?

Bone marrow stromal cells

Know characteristics of B1-B and MZ-B cells

Self renewing in periphery

Harder to study

Dont need replacement from bone marrow

Respond to T-cell independent antigens

What is the effector molecule of adaptive humoral immunity?

antibody

What are the effector functions of humoral immunity, and what do the words and abbreviations mean?

Opsonization: enhances phagocytosis

Neutralization: inactivates and prevents binding

Complement fixation: lysis of pathogen by MAC formation

ADCC: NK cell induced apoptosis

Cell mediated cytotoxicity: recruit NK cells to trigger apoptosis

What is needed for a cell to extravasate at the HEV (general names of molecules and cells)?

Need chemokines to form concentration (depenant “trail”)

Need addressins and homing to get there properly

DO NOT need the dendritic cells because they are doing something different

What 2 things do PRRs on innate cells do?

PRRs coordinate killing of pathogens and recognize general patterns on the surface of a pathogen

Alert adaptive system there is an infection… macrophages alert dendritic cells

Recognize PAMPs and trigger signaling

At what function do APCs improve early in an infection?

APCs early get better at antigen presentation and later they go through apoptosis

Become more effective at antigen processing

What steps does an APC follow from taking up an antigen to presenting it?

1. Antigen uptake > antigen processing > APC migration to lymph nodes > antigen presentation

APCs present antigen in MHCs to _______ cells

CD4+ T-helper cells

How do antigens get transferred to FDCs?

CD169 macrophages to the antigen NON specific cells

Then to the follicular dendritic cells via complement receptors

Which cells are active early in a primary infection? Which only develop later?

• Early: Innate cells (neutrophils, macrophages, DCs, NK), complement

• Later: Adaptive effector cells (CTLs, Th cells), class-switched antibody/plasma cells, memory cells

What signals does a B cell need to activate?

T cells activate B cells through CD40 signaling

There is no CD40-CD40L ligand interaction