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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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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 result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
MHC I; from RER with help of the B2 microglobulin
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Interferon gamma and IL 2

2. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Recom IL 11; thrombocytopenia
IgAs in mothers breast milk!
IgG

3. From where do cytokines come from?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Lymphocytes
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Fab portion

4. Which is the main antibody that provides passive immunity to infants?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IgA
dimer
IgG

5. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Edema and necrosis in that region
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
Th cells fail to produce interferon gamma; a lot of IgE
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

6. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
MHC I; from RER with help of the B2 microglobulin
Superficial inguinal
Anti viral and anti tumor

7. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Hemochromatosis
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IgM

8. hat is the presentation of Jobs syndrome or Hyper IgE?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
except hyperacute

9. What does Interferon alpha and beta do? how?
Its main effect is a defect in Ab opsonization for killing
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

10. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
False! B cell class switching requires a second signal
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

11. What is immune complex disease? give an example.
Pernicious Anemia and Hashimotos
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
...

12. Name two endogenous pyrogens
neutrophilia!
IL 1 and IL 6
The igA found in breast milk
A - B - C; all the D's

13. what secretes IL 4?
pale central germinal centers
Th2; Th1
Basophils! THey want IG E class switch!
Lymphocytes

14. What is serum sickness? give an example.
IL 4
except hyperacute
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

15. What is oprelevkin? and What is it used for?
DM type I
RNA segment reassortment
Wiskott Aldrich syndrome
Recom IL 11; thrombocytopenia

16. what happens in a deficiency of C1 esterase inhibitor? DAF?
MS
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Hereditary angioedema; PNH
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

17. which type of immunity is slow but long lasting? as opposed to...
Anti Ach receptor
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Active; passive - fast but short half life (3 weeks!)
A chemotactic factor for neutrophils

18. How is the antigen loaded onto a MHC II?
Hemochromatosis
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
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

19. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Tetanus - Botulinum - HBV - Rabies
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Wiskott Aldrich syndrome
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

20. __________ are a part of the innate system.
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
NK cells
opsonizes
False! B cell class switching requires a second signal

21. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
heavy chains
By transcytosis
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

22. What does it mean if there are igM in the serum at birth?
MS - hay fever - SLE - goodpastures
Anti Ach receptor
B - T - and NK cells
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

23. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
A - B - C; all the D's
Chronic granulomatous disease
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

24. How does the alternative pathway lead to MAC activation?
In the germinal center of secondary follicles (In the paler center)
Antidote for digoxin intoxication
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

25. which antibody is involved in the primary response or immediate response to an antigen?
Antidote for digoxin intoxication
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IgM

26. What are the autoantibodies for goodpastures syndrome?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Anti alpha subunit 3 of collagen on type IV bm
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

27. What is chronic mucocutaneous candidiasis d/t?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Celiac
T cell dysfunction

28. What is the defect in hyper IgM syndrome? What are the lab results?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
Paracortex
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

29. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
A j chain
Paracortex; viral infection
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

30. 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?
DM type I and RA
lowest concentration
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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

31. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Activate macrophages
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

32. 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?
Daclizumab; prevent ACUTE rejection of renal transplant
A j chain
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IgM and IgA

33. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Cells that stil have weird parts of their membrane that macrophages usually bite off
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

34. What is the general structure of an Ab?
By transcytosis
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
2 heavy chains and two light chains
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

35. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
...
delayed!
Anti Ach receptor

36. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
acute phase reactants
Antibody mediated cytotoxicity; either complement dependent or complement independent
...

37. What lymph node drains the sigmoid colon?
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
Inferior mesenteric
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

38. What links the adaptive and innate immunity?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
isotype
Complement activation (active in both)

39. What is the pathology of acute transplant rejection? is it reversible?
pale central germinal centers
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
If there is class switching and plasma cell production (that is when memory cells are produced)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

40. Describe the Mannose Lectin pathway
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
Cross link
Negative selection

41. What lymph node drains the duodenum - jejunum?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Superior mesenteric
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

42. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
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
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

43. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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

44. What is filgrastim and sargramostim? and 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
IgE
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

45. Give an example of someone who could get hyperacute transplant rejection.
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Anti IF
Previous transfusion; pregnant woman whose fetus had paternal antigens
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

46. What is the clinical use for azathioprine?
Basophils! THey want IG E class switch!
...
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

47. Monomer in circulation - ___ when secreted
Its main effect is a defect in Ab opsonization for killing
Anti Ach receptor
Superficial inguinal
dimer

48. What are the autoantibodies for systemic sclerosis?
isotype
Pernicious Anemia and Hashimotos
Anti topoisomerase
B - T - and NK cells

49. Which are the only two antiinflammatory cytokines?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
TGF beta and IL 10
cannot cross placenta
Immunoflourescent staining of tissue biopsies

50. What lymph node drains the rectum (above the pectinate line)?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
isotype
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
Internal iliac

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USMLE Step 1 Immunology

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