Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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. Name 5 ways Antibody diversity is generated?
Axillary
Anti topoisomerase
Anti Ach receptor
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi

2. What are the symptoms of serum sickness?
encapsulated
Carbohydrate
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IgE; by activating eosinophils

3. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
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
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
pathogenesis

4. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
delayed!
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

5. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
MHC II - B7
Activate macrophages
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Glycoproteins; HLA

6. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Anti viral and anti tumor
Anti mitochondrial
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Fab portion

7. Give three examples of bacteria that use antigenic variation and how.
Not thymus - BM
IgM and IgG
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

8. What is the treatment of acute transplant rejection?
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
encapsulated
Cyclosporine - OKT3
neutrophilia!

9. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
Anemias (esp due to renal failure)
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
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

10. What is three common causes of severe combined immunodef? What is the result of all three?
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)
Activate macrophages
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

11. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
S. aureus - E. Coli - aspergillus
Histamine; post capillary venules - vasodilation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

12. What is the main cytokine released by T cells? What does it do
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Previous transfusion; pregnant woman whose fetus had paternal antigens
Influenza; antigenic shift; antigenic drift
IL 3; supports growth and differentiation of bone marrow stem cells

13. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
Anti smooth muscle
Hemochromatosis

14. What are four results of a splenectomy?
RNA segment reassortment
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
DM type I and RA

15. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Glycoproteins; HLA
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

16. What does it mean if there are igM in the serum at birth?
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
Glycoproteins; HLA
encapsulated

17. IgE has the ___________ in the serum
Activates Th1 helper cells; Macrophages
lowest concentration
Paracortex
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

18. How does the alternative pathway lead to MAC activation?
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IgAs in mothers breast milk!

19. What are C1 - C2 - C3 - C4 important for?
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
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
Superficial inguinal
Viral neutralization of igM and IgG!

20. Which disease is associated with HLA A3?
Liver! (they are proteins circulating in the blood)
Hemochromatosis
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

21. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
DM type I and RA
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

22. What is Aldesleukin? What is it used for
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
...
A recomb cytokine of IL 2; RCC and metastatic melanoma
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

23. 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
Active; passive - fast but short half life (3 weeks!)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

24. is IgM an opsonizer?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Sinusitis - otitis media - pneumonia
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
Negative!

25. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Active; passive - fast but short half life (3 weeks!)

26. Type IV hypersensitivity is i...
not Ab mediated
Celiac
IgG
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

27. What is thrombopoietin used for?
Thrombocytopenia
Antihistone
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Stimulate the liver to release acute phase reactants

28. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Th cells fail to produce interferon gamma; a lot of IgE
Receiving preformed Antibodies
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

29. what characterizes an arthus reaction?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
T cell activation; no with CD 4 or CD 8
Edema and necrosis in that region
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

30. what ensure that a memory response is generated?
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
Interferon gamma; Th1
If there is class switching and plasma cell production (that is when memory cells are produced)
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

31. What lymph node drains the scrotum?
Fab portion
Superficial inguinal
TNF alpha and IL1
RNA segment reassortment

32. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Antidote for digoxin intoxication
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Kill them because they have CD16 on them that recognize the FcG portion
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

33. What lymph node drains the stomach?
Celiac
Paracortex; viral infection
Sinusitis - otitis media - pneumonia
Viral neutralization of igM and IgG!

34. What are the two signals to kill for NK cells?
DM type I and RA
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgE; by activating eosinophils
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

35. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Tetanus - Botulinum - HBV - Rabies
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

36. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

37. what bacteria are a splenectomy patient most susceptible to? why?
Tetanus - Botulinum - HBV - Rabies
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
acute phase reactants
A chemotactic factor for neutrophils

38. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cell activation; no with CD 4 or CD 8
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

39. What are the three types of lymphocytes?
B - T - and NK cells
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
MHC II - B7

40. How is the thymus organized? what happens in each section?
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
Kill them because they have CD16 on them that recognize the FcG portion

41. What are some catalase positive organisms?
...
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
S. aureus - E. Coli - aspergillus
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

42. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Interferon gamma and IL 2
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IL 5

43. What is the marginal zone of the spleen? what happens there?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
IL 15; IL 12 - interferon Beta and interferon alpha
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

44. What are the autoantibodies for wegeners granulomatosis?
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
By transcytosis
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

45. What is an example of a parasite showing antigenic variation?
Anti glutamate carboxylase and anti insulin
Anti Ach receptor
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

46. How do you test for type III hypersensitivity?
Viral neutralization of igM and IgG!
Immunoflourescent staining of tissue biopsies
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
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

47. __________ are a part of the innate system.
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
S. aureus - E. Coli - aspergillus
NK cells

48. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
encapsulated
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

49. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Complement activation (active in both)

50. What is the pathogenesis of acute transplant rejection? When does it occur?
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
...
Superficial inguinal
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after