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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 Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
mesenchymal
Severe pyogenic infections early in life
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

2. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Superficial inguinal
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Paracortex
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

3. which antibody activate mast cells - basophils - and eosinophils?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IgE
...
Daclizumab; prevent ACUTE rejection of renal transplant

4. What are the autoantibodies for sjorgens syndrome?
Tetanus - Botulinum - HBV - Rabies
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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
Anti SS- A (anti RO) and Anti SS- B

5. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

6. Name two endogenous pyrogens
IL 1 and IL 6
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
lowest concentration
The igA found in breast milk

7. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgAs in mothers breast milk!
Antidote for digoxin intoxication
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

8. What are the PALS?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
secondary
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

9. What is recomb gamma interferon used for?
Antidesmoglein
Hemochromatosis
IgE
Chronic granulomatous disease

10. Describe the complement independent Type II hypersenstivity reaction. Give an example.
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
IL 5
active complement pathway
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

11. What is the clinical use for azathioprine?
TLR ad nuclear receptors
Bind FcG for antibody dependent cellular cytotoxicity
...
mesenchymal

12. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
IgM
Carbohydrate
...

13. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Graves
TNF alpha and IL1
Histamine; post capillary venules - vasodilation
Immunoflourescent staining of tissue biopsies

14. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
Alternative splicing of mRNA
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
carboxy terminal

15. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgAs in mothers breast milk!
Glycoproteins; HLA

16. The secondary follicles have __________; primary follicles are dense
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti glutamate carboxylase and anti insulin
Local infection/inflammation; infection of the ln itself; metastasis
pale central germinal centers

17. A lymph node is a ________ lymphoid organ.
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
secondary
Kill them because they have CD16 on them that recognize the FcG portion
Thrombocytopenia

18. What is the main function of IL 12? other than macrophages who else can release IL 12?
Paracortex; viral infection
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

19. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
Thrombocytopenia
...
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

20. describe the classic complement pathway.
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
SP infections

21. what bacteria are a splenectomy patient most susceptible to? why?
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
IgM and IgA
Stimulate the liver to release acute phase reactants
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

22. How is i Th1 helper cell inhibited?
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
Cytokine IL 10 secreted by Th2
Anti smooth muscle
Internal iliac

23. Describe the Mannose Lectin pathway
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
Type IV
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
Para aortic

24. which antibodies can bind complement?
except hyperacute
IgM and IgG
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

25. The Fc region is found on the...
carboxy terminal
Fab portion
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

26. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Chronic granulomatous disease
Activates Th1 helper cells; Macrophages
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

27. What is the white pulp of the spleen?
IL 5
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
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

28. What is a factor that is a predictor for a bad transplantation?
opsonizes
All MHC 1/CD8
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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

29. what characterizes an arthus reaction?
Edema and necrosis in that region
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Inferior mesenteric
Histamine; post capillary venules - vasodilation

30. which B and T cell disorder presents with specifically low IgM?
Activate macrophages
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Wiskott Aldrich syndrome
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

31. What type of side chains are found on Fc region of an antibody?
Severe pyogenic infections early in life
Paracortex; viral infection
Carbohydrate
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

32. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
lowest concentration
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 :(
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

33. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Carbohydrate

34. What lymph node drains the thigh?
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Sinusitis - otitis media - pneumonia
Superficial inguinal

35. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IgE
Anti TSh receptor
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

36. What is a type I hypersensitivity reaction? What is atopic?
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 IF
Viral neutralization of igM and IgG!
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

37. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
S. aureus - E. Coli - aspergillus

38. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgA
Internal iliac

39. What is three common causes of severe combined immunodef? What is the result of all three?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Superficial inguinal
Complement activation (active in both)

40. 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
...
Its main effect is a defect in Ab opsonization for killing
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

41. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
pentamer
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
CD21 on B cells (although there is T cell lymphocytosis in EBV)
C5a

42. What is the pathology seen in chronic transplant rejection?
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
T cell activation; no with CD 4 or CD 8
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Axillary

43. What is the autoantibody for SLE that is nonspecific? Specific?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

44. What is the treatment of acute transplant rejection?
Increases expression of MHC I and MHC II and also activates NK cells
NK cells
Cyclosporine - OKT3
S. aureus - E. Coli - aspergillus

45. What is the mechanism for sirolimus? what else it known as?
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
The igA found in breast milk
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton

46. 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
Basophils! THey want IG E class switch!
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
...

47. What does granulysin do?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

48. What do mature naive B lymphocytes express?
Th2; Th1
IgM and IgD
Steroid responsive nephrotic syndrome
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

49. What is the pathogenesis of acute transplant rejection? When does it occur?
All MHC 1/CD8
Antihistone
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton

50. What are the autoantibodies for autoimmune hepatitis?
A j chain
The igA found in breast milk
Anti smooth muscle
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection