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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.

1. What are the two signals required for T cells? what happens after?
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Carbohydrate
If there is class switching and plasma cell production (that is when memory cells are produced)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

2. The pathogenesis of contact dermatitis is ________ hypersensitivity
Th2; Th1
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
Lymphocytes
type four

3. What are superantigens? give two examples.
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Macrophages - Dendritic cells - B cells

4. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Steroid responsive nephrotic syndrome
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
IL 3; supports growth and differentiation of bone marrow stem cells
opsonizes

5. Only the _______ contribute to the Fc region
Severe pyogenic infections early in life
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Previous transfusion; pregnant woman whose fetus had paternal antigens
heavy chains

6. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Anti mitochondrial
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
TNF alpha and IL1
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h

7. What lymph node drains the duodenum - jejunum?
pentamer
IL 4 - 5 - 10 - 6
Superior mesenteric
Fab portion

8. What does IgA pick up from epithelial cells before being secreted?
Secretory component
Active; passive - fast but short half life (3 weeks!)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Severe pyogenic infections early in life

9. What are MHC's necessary for? By themselves?
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
T cell activation; no with CD 4 or CD 8
mesenchymal
Anti TSh receptor

10. What is the pathology in hyperacute transplant rejection?
active complement pathway
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
CD56
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

11. What is the main function of IL 8?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
A chemotactic factor for neutrophils
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen

12. what bacteria are a splenectomy patient most susceptible to? why?
When you select for which MHC it will have; take out the lymphs that self react
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
Receiving preformed Antibodies

13. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IgG

14. What is a factor that is a predictor for a bad transplantation?
CRP - C3b - IgM
IL 5
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

15. which cytokine inhibits TH2 cells? secreted by who?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Interferon gamma; Th1
Immunosuppression after kidney transplantation
Yes

16. The alternative pathway is the only constutively...
active complement pathway
opsonizes
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur
The patient could become cyanotic in the OR!

17. What is epo used for?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
Antidesmoglein
Anemias (esp due to renal failure)

18. Which MHC presents intracellular peptides? how so?
IL 4 - 5 - 10 - 6
Rheumatic arthritis
MHC I; from RER with help of the B2 microglobulin
Th cells fail to produce interferon gamma; a lot of IgE

19. The two heavy chains of an antibody contribute to the...
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Fab portion
Type IV
lowest concentration

20. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Cyclosporine - OKT3
Liver! (they are proteins circulating in the blood)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

21. What cytokines to Th2 secrete?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 4 - 5 - 10 - 6
Carbohydrate

22. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Anti Ach receptor
Basophils! THey want IG E class switch!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Superficial inguinal

23. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Activates Th1 helper cells; Macrophages
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

24. What are the two signals required for Th1 cells? what happens after then activated?
A j chain
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Alternative splicing of mRNA

25. What happens in a secondary follicle?
Complement activation (active in both)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Hereditary angioedema; PNH
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

26. What is the presentation of common variable immunodef? and What are the labs?
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Interferon gamma and IL 2
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

27. What is the common variable immunodeficiency ? How is it different from Brutons?
Activates Th1 helper cells; Macrophages
MS
Increases expression of MHC I and MHC II and also activates NK cells
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs

28. where do somatic hypermutation and class switching occur?
Axillary
IgM and IgD
Bind FcG for antibody dependent cellular cytotoxicity
In the germinal center of secondary follicles (In the paler center)

29. What is the clinical use for azathioprine?
...
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
IgE; by activating eosinophils
Anti alpha subunit 3 of collagen on type IV bm

30. How fast does it occur?
heavy chains
Anti Jo -1
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
The patient could become cyanotic in the OR!

31. which of the hypersensitivity reactions is not Ab mediated?
Antimicrosomal and antithyroglobulin
Type IV
IL 4
Hereditary angioedema; PNH

32. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anti U1 RNP (ribonucleoprotein)
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen

33. IgE has the ___________ in the serum
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
delayed!
lowest concentration

34. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
T
Anti alpha subunit 3 of collagen on type IV bm
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

35. what cytokine does basophils secrete?
IL 4
Alternative splicing of mRNA
IgAs in mothers breast milk!
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

36. What is the defect in hyper IgM syndrome? What are the lab results?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Anti smooth muscle
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

37. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
NK cells
Glycoproteins; HLA
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi

38. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

39. What are the main symptoms of B cell immunodeficiencies?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
SP infections

40. What are the autoantibodies for autoimmune hepatitis?
pale central germinal centers
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti smooth muscle

41. Which disease is associated with HLA A3?
Hemochromatosis
...
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

42. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Thrombocytopenia
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

43. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Th cells fail to produce interferon gamma; a lot of IgE
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

44. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Secretory component
Hemochromatosis

45. What are the two signals to kill for NK cells?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Chronic granulomatous disease
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

46. What does IL 10 do? who is secreted by?
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
...
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Superficial inguinal

47. What is the main cytokine that activates eosinophils?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
IL 5

48. What are four results of a splenectomy?
Carbohydrate
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
...

49. What do multimeric antibodies require for assembly?
A j chain
2 heavy chains and two light chains
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

50. From where do cytokines come from?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Lymphocytes
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
2 heavy chains and two light chains