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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 is the pathology seen in chronic transplant rejection?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Anti U1 RNP (ribonucleoprotein)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

2. What is the main function of IL 8?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
A chemotactic factor for neutrophils
Local infection/inflammation; infection of the ln itself; metastasis
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

3. In general What are T cells good for?
Anti viral and anti tumor
Kill them because they have CD16 on them that recognize the FcG portion
TNF alpha and IL1
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

4. From where do cytokines come from?
Lymphocytes
Hemochromatosis
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Histamine; post capillary venules - vasodilation

5. A lymph node is a ________ lymphoid organ.
secondary
T cell precursor
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

6. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Severe pyogenic infections early in life
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Delayed type hypersensitivity

7. What are the main symptoms of B cell immunodeficiencies?
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
delayed!
mesenchymal
SP infections

8. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

9. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Pernicious Anemia and Hashimotos
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
pathogenesis

10. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Remove encapsulated bacateria
IgAs in mothers breast milk!
pentamer
Its main effect is a defect in Ab opsonization for killing

11. Only the _______ contribute to the Fc region
Negative!
Superficial inguinal
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
heavy chains

12. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
The patient could become cyanotic in the OR!
Anti TSh receptor

13. IgM can fix complement but...
No because no peptide fragment!
Bind FcG for antibody dependent cellular cytotoxicity
C5a
cannot cross placenta

14. What is the main function of IL 12? other than macrophages who else can release IL 12?
pathogenesis
Wiskott Aldrich syndrome
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Liver! (they are proteins circulating in the blood)

15. what results in symptoms of shock in an acute hemolytic transfusion reaction?
RNA segment reassortment
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
DM type I

16. How is the antigen loaded onto a MHC II?
Anti viral and anti tumor
Popliteal
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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

17. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Anti IF
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)

18. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Interferon gamma; Th1
pentamer
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

19. What lymph node drains the sigmoid colon?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Inferior mesenteric
Anti IF
active complement pathway

20. which of the transplant rejections is antibody mediated? why does it occur?
Activates cytotoxic CD 8 T cells as second signal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
pentamer
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

21. What are the three types of APCs?
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Macrophages - Dendritic cells - B cells
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

22. Which disease is associated withB B27?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

23. What is colostrum?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
The igA found in breast milk
Previous transfusion; pregnant woman whose fetus had paternal antigens

24. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
S. aureus - E. Coli - aspergillus
MHC I; from RER with help of the B2 microglobulin
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

25. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
...
Popliteal
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

26. What is recomb alpha interferon used for?
The igA found in breast milk
mesenchymal
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

27. What are the autoantibodies for goodpastures syndrome?
Receiving preformed Antibodies
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti alpha subunit 3 of collagen on type IV bm
T cell activation; no with CD 4 or CD 8

28. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
except hyperacute
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
lowest concentration
Hereditary angioedema; PNH

29. What is the toxicity of muromonab?
Recom IL 11; thrombocytopenia
Secretory component
lowest concentration
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

30. when can graft versus host disease? What is the result?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
...
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

31. What happens in a deficiency of C3?
Delayed type hypersensitivity
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Its a serine protease that activates apoptosis; NK and CD8

32. Name 5 ways Antibody diversity is generated?
IL 4 - 5 - 10 - 6
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
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

33. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Hereditary angioedema; PNH
Bind FcG for antibody dependent cellular cytotoxicity
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

34. Monomer in circulation - ___ when secreted
dimer
Activates cytotoxic CD 8 T cells as second signal
Its a serine protease that activates apoptosis; NK and CD8
C5a

35. What is Aldesleukin? What is it used for
Cells that stil have weird parts of their membrane that macrophages usually bite off
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
A recomb cytokine of IL 2; RCC and metastatic melanoma
acute phase reactants

36. Which antibodies can be multimeric?
Axillary
SP infections
Remove encapsulated bacateria
IgM and IgA

37. What is the clinical use of Muromonab?
MS
2 heavy chains and two light chains
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
Immunosuppression after kidney transplantation

38. The Fc region is found on the...
carboxy terminal
dimer
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
A j chain

39. What bugs can actually infect the lymph node itself?
Previous transfusion; pregnant woman whose fetus had paternal antigens
cannot cross placenta
MHC class molecules bind to KIRS or CD94 to prevent killing
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

40. which cytokine inhibits TH2 cells? secreted by who?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Interferon gamma; Th1
Paracortex
Activates Th1 helper cells; Macrophages

41. Which diseases are associated with DR2?
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
Antihistone
MS - hay fever - SLE - goodpastures
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

42. hat is the presentation of Jobs syndrome or Hyper IgE?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Wiskott Aldrich syndrome
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

43. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
All MHC 1/CD8
Axillary

44. which antibodies can bind complement?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti U1 RNP (ribonucleoprotein)
CRP - C3b - IgM
IgM and IgG

45. What are the autoantibodies for primary biliary cirrhosis?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
IgE
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
Anti mitochondrial

46. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
...
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
MHC I; from RER with help of the B2 microglobulin
Anti alpha subunit 3 of collagen on type IV bm

47. Describe complement dependent Type II hypersensitivity. Give an example.
not Ab mediated
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
heavy chains
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

48. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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)
Anti SS- A (anti RO) and Anti SS- B

49. What are the cell surface proteins on NK cells?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
...
MHC I - CD16 - CD56
Anti mitochondrial

50. What kinds of receptors activate innate immunity?
Activates Th1 helper cells; Macrophages
TLR ad nuclear receptors
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antibody mediated cytotoxicity; either complement dependent or complement independent