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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 is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
IL 1 and IL 6
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the

2. other than mediating shock - what else does TNF alpha do? who releases it mainly?
...
Activates Th1 helper cells; Macrophages
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Anemias (esp due to renal failure)

3. What does interferon gamma do? What two type of cells does it attack mostly?
secondary
IgG
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

4. How is the antigen loaded onto a MHC II?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Macrophages - Dendritic cells - B cells
delayed!
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II

5. Which type of selection of thymic development provides central tolerance?
Negative selection
Cross link
Anti Jo -1
IL 5

6. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
heavy chains
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

7. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Delayed type hypersensitivity
S. aureus - E. Coli - aspergillus

8. Which cytokines do Th2 release and For what?
Influenza; antigenic shift; antigenic drift
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

9. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Kill them because they have CD16 on them that recognize the FcG portion

10. What are the autoantibodies for drug induced lupus?
IgM and IgG
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
Humoral
Antihistone

11. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)

12. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
False! B cell class switching requires a second signal
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Paracortex; viral infection

13. What are the function of B cells?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Secretory component
Kill them because they have CD16 on them that recognize the FcG portion

14. What can cause a lymph node enlargement?
Liver! (they are proteins circulating in the blood)
Antidote for digoxin intoxication
Para aortic
Local infection/inflammation; infection of the ln itself; metastasis

15. What are the autoantibodies for pernicious anemia?
pentamer
Anti IF
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
SP infections

16. Which HLA's are included in MHC I? MHC II?

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17. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Anti mitochondrial
Negative nitroblue tetrazolium reduction test

18. What lymph node drains the lateral side of the dorsum of the foot?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
The igA found in breast milk
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Popliteal

19. What lymph node drains the sigmoid colon?
Immunoflourescent staining of tissue biopsies
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
Inferior mesenteric
IgAs in mothers breast milk!

20. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Basophils! THey want IG E class switch!
Negative selection
Barrel hoop basement membrane fenestrations

21. Which disease is associated with HLA A3?
not Ab mediated
Hemochromatosis
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
S. aureus - E. Coli - aspergillus

22. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Its main effect is a defect in Ab opsonization for killing
Antimicrosomal and antithyroglobulin
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea

23. What is the toxicity of muromonab?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Popliteal

24. are Th cells involved in trapping of antigens of endotoxin/LPS?
Anti mitochondrial
No because no peptide fragment!
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

25. IgE has the ___________ in the serum
IgM and IgD
Paracortex; viral infection
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
lowest concentration

26. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
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
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

27. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
TNF alpha and IL1
Barrel hoop basement membrane fenestrations
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Chronic granulomatous disease

28. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
except hyperacute
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

29. Leukocyte adhesion defect presents with...
neutrophilia!
Glycoproteins; HLA
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
Superficial inguinal

30. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IgG
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

31. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Secretory component

32. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
Anti viral and anti tumor
Severe pyogenic infections early in life

33. What is three common causes of severe combined immunodef? What is the result of all three?
Glycoproteins; HLA
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

34. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
neutrophilia!
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
not Ab mediated

35. What is the general structure of an Ab?
2 heavy chains and two light chains
Histamine; post capillary venules - vasodilation
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

36. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Anti alpha subunit 3 of collagen on type IV bm
Glycoproteins; HLA
NK cells
Anti Ach receptor

37. What lymph node drains the duodenum - jejunum?
Anti IF
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Superior mesenteric
encapsulated

38. What links the adaptive and innate immunity?
Complement activation (active in both)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor

39. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
IL 1 and IL 6
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
mesenchymal
False! B cell class switching requires a second signal

40. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Paracortex; viral infection
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Antibody mediated cytotoxicity; either complement dependent or complement independent

41. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
IL 1 and IL 6
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
The patient could become cyanotic in the OR!

42. What does IgA pick up from epithelial cells before being secreted?
Secretory component
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
TNF alpha and IL1
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

43. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Thrombocytopenia
The patient could become cyanotic in the OR!
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
T cell precursor

44. What is chronic mucocutaneous candidiasis d/t?
RNA segment reassortment
T cell dysfunction
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Activates Th1 helper cells; Macrophages

45. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
pathogenesis

46. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Anti Ach receptor
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

47. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Barrel hoop basement membrane fenestrations

48. What does IL 2 do?
IgM and IgG
Activates cytotoxic CD 8 T cells as second signal
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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

49. What lymph node drains the stomach?
Bind FcG for antibody dependent cellular cytotoxicity
Anti U1 RNP (ribonucleoprotein)
Anemias (esp due to renal failure)
Celiac

50. How is sirolimus different from tacrolimus?
MHC II - B7
IL 4
MHC class molecules bind to KIRS or CD94 to prevent killing
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)