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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 happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Interferon gamma; Th1
Anti Ach receptor
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
A - B - C; all the D's

2. What is the main function of IL 12? other than macrophages who else can release IL 12?
S. aureus - E. Coli - aspergillus
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
The patient could become cyanotic in the OR!
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

3. 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?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
mesenchymal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

4. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
mesenchymal
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
Antibody mediated cytotoxicity; either complement dependent or complement independent

5. where do NK cells develop?
Anti U1 RNP (ribonucleoprotein)
Not thymus - BM
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

6. which cytokine inhibits TH2 cells? secreted by who?
Axillary
Interferon gamma; Th1
Inferior mesenteric
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

7. Which is the main antibody in the delayed or secondary response to an antigen?
neutrophilia!
Its main effect is a defect in Ab opsonization for killing
IgG
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

8. which antibody is involved in the primary response or immediate response to an antigen?
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
Carbohydrate
Edema and necrosis in that region
IgM

9. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
TLR ad nuclear receptors
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
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

10. What is the presentation of Brutons agammaglobulinemia?
active complement pathway
Macrophages - Dendritic cells - B cells
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Its a serine protease that activates apoptosis; NK and CD8

11. What are the autoantibodies for graves?
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
MHC I - CD16 - CD56
Anti TSh receptor
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

12. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
...
Cross link
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

13. In thymic development - What is the positive selection? negative selections?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
When you select for which MHC it will have; take out the lymphs that self react
Immunoflourescent staining of tissue biopsies
Antibody mediated cytotoxicity; either complement dependent or complement independent

14. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
A chemotactic factor for neutrophils
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Barrel hoop basement membrane fenestrations
Anti Ach receptor

15. What are the two signals required for T cells? what happens after?
IL 5
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
active complement pathway

16. The two heavy chains of an antibody contribute to the...
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Fab portion
opsonizes

17. which B and T cell disorder presents with specifically low IgM?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Chronic granulomatous disease
Bind FcG for antibody dependent cellular cytotoxicity
Wiskott Aldrich syndrome

18. What are the three types of lymphocytes?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
B - T - and NK cells
cannot cross placenta
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)

19. What are the autoantibodies for goodpastures syndrome?
Anti Ach receptor
MHC class molecules bind to KIRS or CD94 to prevent killing
Activates Th1 helper cells; Macrophages
Anti alpha subunit 3 of collagen on type IV bm

20. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
Fab portion
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected 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

21. which antibodies prevent antigens from binding mucosal surfaces?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IgA
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

22. What is the clinical use for azathioprine?
DM type I
...
Superficial inguinal
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

23. what prevents NK cells from killing normal cells if their default is to kill?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC class molecules bind to KIRS or CD94 to prevent killing
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
lowest concentration

24. What are the PALS?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Recom IL 11; thrombocytopenia
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IgE

25. In general What are T cells good for?
Popliteal
Anti viral and anti tumor
Active; passive - fast but short half life (3 weeks!)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

26. What does IL 4 do?
dimer
Anti IF
Acts as second signal on B cells to induce class switching to IgE and IgG
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

27. what happens in a deficiency of C1 esterase inhibitor? DAF?
When you select for which MHC it will have; take out the lymphs that self react
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
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

28. Which helper T cells' development is induced by IL 4? IL 12?
Axillary
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Th2; Th1
lowest concentration

29. 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?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Fc
except hyperacute
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

30. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
T
encapsulated
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

31. The MALT/GALT are not...
Alternative splicing of mRNA
encapsulated
A chemotactic factor for neutrophils
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

32. What cytokines are released by Th1 cells?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Interferon gamma and IL 2
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx

33. is IgM an opsonizer?
acute phase reactants
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Anti Ach receptor
Negative!

34. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Antidesmoglein
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

35. what secretes IL 4?
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)
Basophils! THey want IG E class switch!
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Antibody mediated cytotoxicity; either complement dependent or complement independent

36. A lymph node is a ________ lymphoid organ.
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Fab portion
Th2; Th1
secondary

37. What is the main function of interferons?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Complement activation (active in both)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

38. What does it mean if there are igM in the serum at birth?
The patient could become cyanotic in the OR!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
By transcytosis

39. What are the main Cell surface proteins on T cells?
T cell activation; no with CD 4 or CD 8
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

40. Which antibodies can be multimeric?
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
T cell precursor
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

41. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
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
Activate macrophages
Secretory component

42. What is the common variable immunodeficiency ? How is it different from Brutons?
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
IL 3; supports growth and differentiation of bone marrow stem cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Recom IL 11; thrombocytopenia

43. Which disease is associated with DR7?
Glycoproteins; HLA
encapsulated
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Steroid responsive nephrotic syndrome

44. What type of side chains are found on Fc region of an antibody?
C5a
Fc
MHC I; from RER with help of the B2 microglobulin
Carbohydrate

45. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

46. which of the hypersensitivity reactions is not Ab mediated?
Type IV
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti topoisomerase
Immunosuppression after kidney transplantation

47. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
MS - hay fever - SLE - goodpastures
Anti TSh receptor
A - B - C; all the D's
...

48. What does Interferon alpha and beta do? how?
Interferon gamma; Th1
IgM and IgG
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Internal iliac

49. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
T cell dysfunction

50. How does igA cross the epithelium?
Graves
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
By transcytosis

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USMLE Step 1 Immunology

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