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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 4 do?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 1 and IL 6
IL 15; IL 12 - interferon Beta and interferon alpha

2. What are the symptoms of serum sickness?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
DM type I and RA

3. Monomer in circulation - ___ when secreted
dimer
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
B - T - and NK cells
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

4. What is the main cytokine released by T cells? What does it do
Receiving preformed Antibodies
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IL 3; supports growth and differentiation of bone marrow stem cells
The igA found in breast milk

5. describe the classic complement pathway.
MS
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

6. 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?
Activate macrophages
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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

7. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Chronic granulomatous disease
cannot cross placenta
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
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

8. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
type four
Liver! (they are proteins circulating in the blood)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

9. where do NK cells develop?
Its a serine protease that activates apoptosis; NK and CD8
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
Not thymus - BM
Superior mesenteric

10. What is the presentation of Brutons agammaglobulinemia?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
A j chain
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

11. What is the most common selective Ig deficiency? What is the presentation?
Yes
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

12. What bugs can actually infect the lymph node itself?
Anti alpha subunit 3 of collagen on type IV bm
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

13. What are the autoantibodies for goodpastures syndrome?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anti alpha subunit 3 of collagen on type IV bm

14. What is the general structure of an Ab?
MS
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
2 heavy chains and two light chains
pathogenesis

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

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16. What are the function of B cells?
pentamer
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

17. What lymph node drains the stomach?
Celiac
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti topoisomerase
Severe pyogenic infections early in life

18. What are the autoantibodies for myasthenia gravis?
S. aureus - E. Coli - aspergillus
Anti Ach receptor
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anti glutamate carboxylase and anti insulin

19. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
heavy chains
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

20. can igG cross the placenta?
IgG
Yes
isotype
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

21. 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!
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
TLR ad nuclear receptors
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

22. What is serum sickness? give an example.
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
MHC I; from RER with help of the B2 microglobulin

23. What lymph node drains the upper limb?
Axillary
Barrel hoop basement membrane fenestrations
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
type four

24. IgG...
opsonizes
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Viral neutralization of igM and IgG!
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

25. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Rheumatic arthritis
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

26. What is colostrum?
The igA found in breast milk
Type IV
Antidesmoglein
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

27. What is immune complex disease? give an example.
Active; passive - fast but short half life (3 weeks!)
Superior mesenteric
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

28. 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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Axillary
A j chain

29. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
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
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
pathogenesis

30. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Hereditary angioedema; PNH
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
Internal iliac

31. which antibodies prevent antigens from binding mucosal surfaces?
IgA
Activates Th1 helper cells; Macrophages
Antihistone
opsonizes

32. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Anti viral and anti tumor
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
Anti mitochondrial
Daclizumab; prevent ACUTE rejection of renal transplant

33. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Hereditary angioedema; PNH
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
MS - hay fever - SLE - goodpastures

34. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
...
Thrombocytopenia
Lymphocytes
All MHC 1/CD8

35. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
By transcytosis
S. aureus - E. Coli - aspergillus
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

36. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IL 1 and IL 6
mesenchymal
Liver! (they are proteins circulating in the blood)

37. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
TGF beta and IL 10
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IgM and IgG

38. Which disease is associated with DR7?
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!
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
Steroid responsive nephrotic syndrome
Increases expression of MHC I and MHC II and also activates NK cells

39. The ______ in the BM are DN - the DP are in the cortex of thymus
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
T cell precursor
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 :(
Severe pyogenic infections early in life

40. What are some sinopulmonary infections?
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
Sinusitis - otitis media - pneumonia
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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

41. IgM can fix complement but...
cannot cross placenta
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
Immunosuppression after kidney transplantation
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

42. What is a factor that is a predictor for a bad transplantation?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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

43. What is the presentation of hyperIgM syndrome?
pale central germinal centers
Severe pyogenic infections early in life
IL 3; supports growth and differentiation of bone marrow stem cells
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

44. Which are the only two antiinflammatory cytokines?
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
Anti alpha subunit 3 of collagen on type IV bm
IgE
TGF beta and IL 10

45. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Fc
By transcytosis
dimer

46. How does complement link innate and adaptive?
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

47. How is the thymus organized? what happens in each section?
Influenza; antigenic shift; antigenic drift
Previous transfusion; pregnant woman whose fetus had paternal antigens
Bind FcG for antibody dependent cellular cytotoxicity
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

48. What are howell jolly bodies?
Not thymus - BM
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

49. What lymph node drains the sigmoid colon?
except hyperacute
Inferior mesenteric
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
TLR ad nuclear receptors

50. What is chronic mucocutaneous candidiasis d/t?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Graves
T cell dysfunction