First Aid Immunology

Front 1

Where are T Cells found in the spleen?

Back 1

In the periarteriolar lymphatic sheath (PALS).

Front 2

What is found at the marginal zone of the spleen?

Back 2

The marginal zone is in between the white and red pulp and contains macrophages and specialized B cells, and is where antigen presenting cells capture blood-borne antigens for recognition by lymphocytes.

Front 3

What is the effect of splenic dysfunction?

Back 3

There will be an increase in susceptibility to encapsulated organisms due to a decrease in IgM release and opsonization.

Front 4

What are the blood findings after splenectomy?

Back 4

Howell-Jolly bodies, target cells, thrombocytosis and lymphocytosis.

Front 5

What's the embryological origin of the thymus?

Back 5

The third pharyngeal pouch.

Front 6

What do Toll-like receptors bind to abs what does it activate?

Back 6

It binds to pathogen -associated molecular patterns (PAMP) and activates NF-kB.

Front 7

What cytokynes activate NK cells?

Back 7

IL-2 & 12, & IFN alpha and beta

Front 8

What cytokine activates monocytes and macrophages?

Back 8

IFN-gama

Front 9

What is IPEX syndrome?

Back 9

This is an autoimmune disease due to dysregulation of the Regulatory T cells. It is caused by a genetic deficiency in FOXP3 leading to an enteropathy, endocrinopathy, nail dystrophy, dermatitis, and other autoimmune dermatologic conditions.

Front 10

What interaction between B and T cells are necessary for class switching?

Back 10

CD40 on B cell with CD40L on T cell.

Front 11

What is the difference between thymus-dependent and thymus-independent antigens?

Back 11

For the thymus-dependent, there is a protein component to the antigen which illicits a humoral response. For the thymus-independent, there is no protein, such as a lipopolysaccharide of gram negative bacteria, and thus there is no MHC presentation.

Front 12

What type of bacteria do the membrane attack complex of compliments attack?

Back 12

Gram negative bacteria.

Front 13

What complement acts as a neutrophil chemotaxis?

Back 13

C5a

Front 14

What molecules act as the primary opsonins in bacterial defense?

Back 14

C3b and IgG

Front 15

What are the complement inhibitors?

Back 15

Decay-accelerating factor (DAF, aka CD55) and C1 esterase inhibitor.

Front 16

What is the effect of early complement deficiencies (C1-4)?

Back 16

Increased pyogenic sinus and respiratory tract infections.

Front 17

A deficiency in which complement proteins would specifically result in increased susceptibility to recurrent Neisseria infection?

Back 17

C5-9

Front 18

Deficiency of what complement regulatory protein results in hereditary angioedema?

Back 18

C1 esterase inhibitor deficiency.

Front 19

What is the cause of Paroxysmal Nocturnal Hemoglobinuria?

Back 19

A defect in the PIGA gene preventing the formation of anchors for complement inhibitors. It causes complement mediated lysis of RBCs

Front 20

What cytokines activate the endothelium to express adhesion molecules?

Back 20

IL-1 & TNF-alpha

Front 21

What cytokines causes fever?

Back 21

IL-1&6, and TNF-alpha

Front 22

What cytokine causes growth and differentiation of bone marrow stem cells?

Back 22

IL-3

Front 23

What is the function of Interferon-gamma?

Back 23

Release due to IL-12, causing activation of NK cells and Th1 cells, stimulating macrophages to kill phagocytosed pathogens. It also inhibits the differentiation of Th2 cells.

Front 24

What is the function of IL-4?

Back 24

It causes the differentiation of Th2 cells and allows class switch of B-cells to IgE and IgG

Front 25

What cytokine causes activation of Th1 cells?

Back 25

IL-12

Front 26

What cytokine causes stimulation of B cells to produce IgA?

Back 26

IL-5

Front 27

What cytokine attenuates inflammation?

Back 27

IL-10

Front 28

What is lactoferrin?

Back 28

It's a protein that inhibits microbial growth via iron chelation.

Front 29

What is Anergy?

Back 29

The state during which a cell cannot become activated by exposure to its antigen.

Front 30

What vaccines are given live attenuated?

Back 30

Adenovirus, polio, varicella, smallpox, BCG, Yellow fever, Influenza, MMR, and Rotavirus.

Hint 30

Attention! Please Vaccinate Small, Beautiful Young Infants with MMR Regularly!

Front 31

What organisms are given as killed or inactivated vaccines?

Back 31

Rabies, influenza, Polio (stalK), and hepatitis A.

Hint 31

RIP Always.

Front 32

What is the subunit vaccine type?

Back 32

These include only the antigen that best stimulate the immune response.

Front 33

Describe the Toxoid vaccine type?

Back 33

This is the addition of denatured bacterial toxins with an intact receptor binding site. This stimulates Ab against the toxins.

Front 34

What is tryptase?

Back 34

That is a marker of mast cell activation during type one hypersensitivity reactions.

Front 35

How do you test for type one hypersensitivity?

Back 35

The skin test or blood tests (ELISA) for allergen-specific IgE.

Front 36

What is the function of RhoGAM?

Back 36

It is given to mothers to prevent erythroblastosis fetalis.

Front 37

What is the cause and effect of Bruton agammaglobinuria?

Back 37

It is caused by a mutation in BTK, a tyrosine kinase gene needed for B cell maturation. There will therefore be no mature B cells in the blood and decreased Ig. There will be recurrent bacterial and enterovirus infections.

Front 38

A decrease level of plasma cells and Ig due to defective B cell differentiation, along with increased autoimmunity, describes which condition?

Back 38

Common variable immunodeficiency.

Front 39

What is DiGeorge Syndrome?

Back 39

It is a 22q11 deletion leading to the failure to develop the third and forth pharyngeal pouch. This leads to parathyroid and thymus aplasia. So there will be hypocalcemia, leading to tetani, recurrent viral and fungal infections due to T cell deficiency, and conotruncal abnormalities.

Front 40

What is the cause of Job Syndrome (hyper IgE Syndrome)?

Back 40

It is caused by a deficiency of Th17 cells due to a STAT3 mutation, causing increase release of of IgE and eosinophil production, and impaired recruitment of neutrophils.

Front 41

What are the symptoms of Job Syndrome?

Back 41

Coarse Facies, cold staphylococcus Abscesses, retained primary Teeth, increased IgE, & Dermatological problems (eczema). There is also bone fractures from minor trauma.

Hint 41

FATED

Front 42

What is Chronic mucocutaneous candidiasis?

Back 42

This is an absent T-cell response to candida agents due to congenital defects in IL-17 or IL-17 receptors.

Front 43

What Antibodies are deficient in Ataxia Telangiectasia?

Back 43

IgA, IgG, and IgE.

Front 44

What is the most common cause of Hyper-IgM Syndrome?

Back 44

Defective CD40L on Th cells leading to a defect in class switching.

Front 45

What disease is caused by WASp gene mutations and what are the symptoms?

Back 45

Wiskott-Aldrich Syndrome.

WATER: Wiskott-Aldrich - Thrombocytopenia, Eczema, and Recurrent infections.

Front 46

What is the cause of leukocyte adhesion deficiency type 1?

Back 46

A defect in CD18 preventing the leukocytes from adhering to integrins

Front 47

What is the disease and symptoms seen with a defect in the lysosomal trafficking regulator gene (LYST)?

Back 47

Chediak-Higashi Syndrome.

PLAIN- Progressive neurodegeneration, Lymphohistiocytosis, Albinism (partial), recurrent pyogenic Infections, and peripheral Neuropathy.

Hint 47

CH-PLAIN

Front 48

What is the defect in Chronic granulomatous disease?

Back 48

NADPH oxidase causing increased susceptibility to catalase positive organisms.

Front 49

The production of what substance is inhibited by the action of the drugs cyclosporine and tacrolimus.

Back 49

Calcineurin, which results in the prevention of IL-2 transcription.

Front 50

What is the main toxicity of calcineurin inhibitors?

Back 50

Nephrotoxicity.

Front 51

Other than tacrolimus, what other drug binds to FKBP to block T-cell activation (along with B-cell differentiation) by preventing response to IL-2?

Back 51

The mTOR inhibitor: Sirolimus (Rapamycin).

Front 52

What is the action of Basiliximab in immunosuppression?

Back 52

It blocks IL-2 receptors.

Front 53

What is the MOA of azathioprine?

Back 53

It is the precursor of 6 mercaptopurine, which blocks PRPP amidotransferase, an enzyme in purine synthesis.

Front 54

What is a side effect of azathioprine and what drug does it interacts with?

Back 54

It causes bone marrow suppression leading to pancytopenia, and it interacts with allopurinol.

Front 55

What is the MOA of Mycophenolate (Mofetil).

Back 55

It blocks IMP dehydrogenase.

Front 56

What are the two colony stimulating factors given during leucopenia?

Back 56

Filgrastim (G-CSF) & Sargramostim (GM-CSF).

Front 57

What thrombopoetin analog and receptor agonists can be given during autoimmune thrombocytopenia?

Back 57

Romiplostim and eltrombopag respectively.

Front 58

What is Aldesleukin?

Back 58

It is IL-2 given during renal cell carcinoma and metastatic melanoma.