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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 does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
In the germinal center of secondary follicles (In the paler center)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti glutamate carboxylase and anti insulin

2. What are the autoantibodies for primary biliary cirrhosis?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
T cell precursor
Anti mitochondrial
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

3. Describe the Mannose Lectin pathway
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Its a serine protease that activates apoptosis; NK and CD8
Cross link

4. What are the main symptoms of T cell immunodeficiencies?
CRP - C3b - IgM
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Activate macrophages

5. What is the marginal zone of the spleen? what happens there?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
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
Humoral

6. What are the two signals to kill for NK cells?
lowest concentration
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
MHC class molecules bind to KIRS or CD94 to prevent killing
IgM and IgA

7. which of the transplant rejections is antibody mediated? why does it occur?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MHC I - CD16 - CD56

8. IgG...
opsonizes
dimer
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

9. What is the most common example of passive immunity?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IgA
IgAs in mothers breast milk!
Liver! (they are proteins circulating in the blood)

10. What is the mechanism for sirolimus? what else it known as?
TNF alpha and IL1
IgA
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

11. Only the _______ contribute to the Fc region
heavy chains
Anti glutamate carboxylase and anti insulin
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

12. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Thrombocytopenia
Paracortex; viral infection
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

13. What is the pathology of acute transplant rejection? is it reversible?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
T cell dysfunction

14. Type Iv hypersensitivity is...
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
delayed!
B - T - and NK cells

15. What is the clinical use for azathioprine?
...
Wiskott Aldrich syndrome
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
Bind FcG for antibody dependent cellular cytotoxicity

16. How do you test for chronic granulomatous disease?
MS - hay fever - SLE - goodpastures
Anti TSh receptor
Negative nitroblue tetrazolium reduction test
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

17. What are MHC's necessary for? By themselves?
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
T cell activation; no with CD 4 or CD 8
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Superficial inguinal

18. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Steroid responsive nephrotic syndrome
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

19. Which disease is associated with HLA A3?
isotype
active complement pathway
Receiving preformed Antibodies
Hemochromatosis

20. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
IgG
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
opsonizes

21. The ______ in the BM are DN - the DP are in the cortex of thymus
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
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 cell precursor
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

22. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Alternative splicing of mRNA
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anemias (esp due to renal failure)

23. Which diseases are associated with DR4?
Anti Jo -1
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
DM type I and RA
active complement pathway

24. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC II - B7
The patient could become cyanotic in the OR!

25. What is the pathogenesis of HyperIgE syndrome? What are the labs?
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
IgM and IgD
Antibody mediated cytotoxicity; either complement dependent or complement independent
Th cells fail to produce interferon gamma; a lot of IgE

26. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Liver! (they are proteins circulating in the blood)
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!

27. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Cross link
T cell dysfunction
IgG

28. What are the autoantibodies for Mixed connective tissue disease?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti U1 RNP (ribonucleoprotein)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Acts as second signal on B cells to induce class switching to IgE and IgG

29. What does CD16 on NK cells do?
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
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
Bind FcG for antibody dependent cellular cytotoxicity
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

30. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Its a serine protease that activates apoptosis; NK and CD8
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

31. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Popliteal
neutrophilia!

32. Name two endogenous pyrogens
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Immunosuppression after kidney transplantation
IL 1 and IL 6
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

33. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Para aortic
...
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

34. What are the autoantibodies for other vasculitides?
cannot cross placenta
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

35. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Negative!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

36. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Pernicious Anemia and Hashimotos
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Hemochromatosis
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!

37. What does granzyme do? who secretes it?
Anti alpha subunit 3 of collagen on type IV bm
Its a serine protease that activates apoptosis; NK and CD8
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
...

38. which antibodies can bind complement?
IgG
IgM and IgG
Increases expression of MHC I and MHC II and also activates NK cells
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

39. What are the autoantibodies for polymyositis and dermatomyositis?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Anti Jo -1
Antimicrosomal and antithyroglobulin

40. IgM can fix complement but...
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
cannot cross placenta
IL 3; supports growth and differentiation of bone marrow stem cells
Inferior mesenteric

41. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
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
delayed!
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

42. What is the most common selective Ig deficiency? What is the presentation?
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

43. Describe complement dependent Type II hypersensitivity. Give an example.
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
Thrombocytopenia
...
When you select for which MHC it will have; take out the lymphs that self react

44. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Steroid responsive nephrotic syndrome

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

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46. What lymph node drains the scrotum?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Superficial inguinal
MS
Immunosuppression after kidney transplantation

47. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Anti TSh receptor

48. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
When you select for which MHC it will have; take out the lymphs that self react
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

49. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Liver! (they are proteins circulating in the blood)
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

50. where are complements produced?
pathogenesis
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Lymphocytes
Liver! (they are proteins circulating in the blood)