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IHO FINAL > Immunology Part II > Flashcards

Immunology Part II Flashcards

1
Q

What are five common deficiencies related to Innate Immunity?

A
  1. Congenital Neutropenia
  2. Chronic Granulomatous disease
  3. Leukocyte Adhesion Deficiency (LAD)
  4. Complement Defects (various)
  5. Chediak-Higashi Syndrome
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2
Q

What happens in Congenital Neutropenia?

A

(still have some innate immunity protection due to NK cells)

  • Lack of GM-CSF
  • Frequent bacterial infections
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3
Q

What happens in Chronic Granulomatous Disease?

A
  • Inability to produce hydrogen peroxide and hypochlorus acid
  • Inability to kill phagocytosed bacteria
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4
Q

What is Leukocyte Adhesion Deficiency (LAD)?

A
  • Lack of intern subunit, the common beta chain
  • Inability to recruit innate immune cells to site of inflammation
  • Increased susceptibility to bacterial, fungal and viral infections
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5
Q

What are Complement Defects (various)?

A
  • Increased susceptibility to bacterial infections

- Reduced ability to remove immunocomplexes (bound to surface of bacterial cells)

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6
Q

What is Chediak-Higashi Syndrome?

A
  • Defect in gene LYST (CHS1), a lysosomal trafficking gene that affects lysosomes and melanosomes
  • Increased susceptibility to bacterial infections
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7
Q

What are Defensins and Cathelicidins?

A
  • Major families of antimicrobial peptides

- Widely expressed in a variety of epithelial cells and sometimes in leukocytes

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8
Q

What do Defensins and Cathelicidins do?

A
  • Role in innate immunity through antimicrobial, chemotactic and regulatory activities
  • Protect against bacteria, fungi, viruses and parasites
  • 100s of defensin proteins have been identified in nature!
  • Interact with microbial cell membrane components to increase cellular permeability resulting in cell death
  • They also act to modulate the inflammatory response
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9
Q

What are Cathelicidins?

A

(CATionic HELIcal bacteriCIDal proteIN) are alpha-helical peptides
-Human cathelicidin LL37 is highly expressed by PMNs and numerous mucosal and epithelial cell types

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10
Q

What are Defensins?

A

Beta-strand peptides connected by disulfide bonds

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11
Q

How is the acute inflammatory response activated?

A
  1. Pathogen crosses or causes damage to physical barrier
  2. PAMPs and/or DAMPs get released
  3. TLR on resident macrophage gets stimulated (reprogrammed)
  4. Macrophage releases chemokines (IL-1 and TNF-alpha)
  5. TNF-alpha from macrophage stimulates endothelial cell to express E-selectin on its surface.
  6. If E-selectin is expressed and there is an inflammatory response, leukocyte will slow down in blood vessel and bind the E-selectins!
  7. Leukocyte migration occurs!
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12
Q

How does Leukocyte migration occur?

A

a. Rolling
b. Tethering to E-selectins –> mediated by CD15 and E-selectin
c. Adhesion (more stable interaction between leukocyte and surface of the cell)
d. Migration

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13
Q

How does a leukocyte get “pulled into” the cell?

A
  1. Th1 supplies interferon (IFN-gamma) to induce M1 (angry, phagocytosing) state in Macrophage.
  2. Endothelial cells make ICAM-1
    - Lymphocytes make CR3 & CFA1 [These bind ICAM-1 and make a more permanent interaction]
  3. Cell can move ICAM-1 into the tissue, bringing the cell in with it! [can also alter vascular permeability to Inc. migration]
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14
Q

What should you know about MHC I?

A
  • Antigen synthesized in cell/from cell infections
  • Recognized by CD8 cells
  • Expressed on all cells except RBCs (may play role in malaria persistence)
  • CD8 Surveys every cell in body and makes suits doing what it should be & if pathogen present will induce phagocytosis
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15
Q

What should you know about MHC II?

A
  • Antigens are products of phagocytosis
  • Recognized by CD4+ cells
  • Expressed on monocytes/macrophages, DC, B cells and epithelial cells of thymus
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16
Q

What are the T cell markers?

A
  • TCR (alpha-beta & gamma-delta) [antigen receptor]
  • CD3 [part of TCR complex]
  • Some have CD4, CD8, CD23
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17
Q

What are the B cell markers?

A
  • BCR = Ig (Immunoglobulin) antigen receptor

- CD1, CD19, CD20, CD23, CD40, CD79a (part of BCR complex), CD79b (part of BCR complex)

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18
Q

What are Th1 cells?

A

-Recognize antigen and make lymphokine that attracts thousands of macrophages (the heavy-duty phagocytes) to the area where antigen has been recognized. This intense inflammation can wipe out serious infection (or a transplanted kidney!)

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19
Q

What are Th2 cells?

A
  • Stimulate macrophages to become ‘alternately activated’, able to function in walling-off pathogens and promoting healing, a process that usually takes place after the pathogen-killing Th1 response
  • They are very important in parasite immunity
20
Q

What are Th17 cells?

A
  • Similar to Th1 in that their main role is to cause focused inflammation, although they are more powerful than Th1
  • They have been implicated in many serious forms of autoimmunity
21
Q

What are Tfh cells?

A

Stimulated by antigen and migrate from T cell areas of lymph nodes into the B cell follicles, where they help B cells get activated and make the IgM, IgG, IgE and IgA antibody subclasses.

22
Q

What are Treg cells?

A

Make cytokines that suppress the activation and function of Th1, Th17 and Th2 cells, so they keep the immune response in check. They are part of the Th family.

23
Q

What do CTLs do?

A

Destroy any body cell they identify as bearing a foreign or abnormal antigen on its surface.

24
Q

What do Cytotoxic T cells do?

A

Examine surfaces of incoming dendritic cells for presenting antigenic fragments. They are looking for fragments on a different class of antigen-presenting molecule, called MHC Class I which is on all cells (except RBC)

25
Q

What are the four steps involved in cytotoxic killing?

A
  1. If activated, a clone of the CD8+ T cells gets expanded and the daughters circulate in large numbers thoughout the body.
  2. When one of the daughters of a stimulated CD8+ T cell binds a cell showing its “activation” peptide, the T cell delivers a lethal hit to that cell by signaling the target cell to commit suicide through apoptosis.
  3. The target cell’s nucleus disintegrates and the cell dies.
  4. The activated killer T cell then is free to find more targets. This is a great way to eliminated infected cells.
26
Q

What are the five common B cell disorders?

A
  • X-linked Agammaglobulinemia
  • CD40 ligand deficiency
  • Activation-Induced Cytidine Deaminase Deficiency
  • Common Variable Immunodeficiency
  • Omenn Syndrome
27
Q

What is X-linked Agammaglobulinemia?

A

An absence of B lymphocytes

28
Q

What is CD40 ligand deficiency?

A

Failure of immunoglobulin class switching

29
Q

What is Activation-Induced Cytidine Deaminase Deficiency?

A

Failure of immunoglobulin class switching

30
Q

What is Common Variable Immunodeficiency?

A

A failure to produce antibodies against particular antigens

31
Q

What is Omenn syndrome?

A

VDJ recombination failure. Cannot produce BCRs or TCRs.

32
Q

What are five common T Cell Disorders?

A 
X-linked Severe Combined Immunodeficiency 
Omenn Syndrome
DiGeorge Syndrome
Hemophagocytic Lymphohistiocytosis
IPEX
33
Q

What is X-linked Severe Combined Immunodeficiency?

A

A failure to produce mature T lymphocytes

34
Q

What is Omenn Syndrome?

A

VDJ recombination failure. Cannot produce BCRs or TCRs.

35
Q

What is DiGeorge Syndrome?

A

Failure of thymus to develop correctly

36
Q

What is IPEX?

A

Failure of peripheral tolerance due to defective regulatory T cells.

37
Q

What are the parts of the B cell receptor?

A

Heavy chain, light chain

  • Has constant and variable region
  • Variable region binds epitopes
38
Q

What is IgD?

A

Main form of antibody inserted into B cell membranes as their antigen receptor, which seems to be its only biological role

39
Q

What allows the leukocyte to be moved from venule into the tissue?

A
  • The endothelial cell increases expression of ICAM-1

- Then the leukocyte produces CR3 which binds to more ICAM-1 and allows movement across membrane

40
Q

What leukocyte CD binds E-selectin?

A

CD15 - this holds leukocytes in place and they get further instructions in form of IL-8

41
Q

8 month child, faint pink maculopapular rash covering abdomen and limbs. Rash appeared this morning. Early in the week child had a fever for three day, which peaked at 103F. Fever resolved 2 days ago. What is this disease?

A

HHV-6 and HHV-7
Treat with supportive treatment (antipyretics and fluids). - Ganciclovir for immunocompromised
[Not parvo because fever isn’t high enough and parvo fever doesn’t resolve before rash starts]

42
Q

21 yr old male, lymphadenopathy, fever, pharyngitis appeared four days ago. Analysis of blood reveals large cells with dense nuclear inclusions that have an “owl’s eye” appearance. Heterophile antibodies are NOT present in serum. What is this disease?

A
  • CMV - Cytolomegalovirus!! - Large cell, owls eyes

- Can remain latent in cells of the monocyte-macrophage lineage

43
Q

What does EBV increase the risk of?

A

Burkitts Lymphoma

44
Q

What protein does Kaposi’s Sarcoma Herpes Virus encode?

A

vCyclin, a protein like human cyclin D - it phosphorylates and inactivates RB. Then E2F can constitutively activates genes!!
-Relative to an uninfected cell, a cell infected with KSHC would be expected to have increased transcription of E2F regulated genes.

45
Q

2 yr old with rash. Mother reported he was irritable and had mild fever last night. Rash appeared this morning. Temp = 100 deg. Bring red rash on cheeks and forehead. Rash feels warm. Patient’s symptoms are caused by. . .

A 
Parvovirus B19 (a virus) that can cause transient aplastic crisis in patients with underlying anemia. 
= Bright red, slapped cheek look, mild fever = Parvovirus B19
46
Q

What are the properties of the virus Parvovirus B19?

A

HHV-5, Single stranded DNA, Non-enveloped

Tropism = Erythroid Progenitor Cells!

47
Q

24 yr old male - headache, malaise, generalized myalgia - appeared 5 days ago. He reported that the fever appeared at the onset of symptoms, resolved for 2 days and returned - “saddleback” pattern. Patients blood showed neutropenia, thrombocytopenia, mild anemia. Lymphocytes are in his CSF. Bitten by tick in Wyoming. What is this disease?

A

Colorado Tick Fever Virus.

Non-Enveloped (arthropod vector) virus with segmented genome, darn, no envelope, icosahedral, saddle-back fever pattern.

IHO FINAL (12 decks)

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