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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 main function of IL 8?
Its main effect is a defect in Ab opsonization for killing
Anti TSh receptor
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
A chemotactic factor for neutrophils

2. What is recomb gamma interferon used for?
pale central germinal centers
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Chronic granulomatous disease
No because no peptide fragment!

3. What are the autoantibodies for primary biliary cirrhosis?
IgM and IgA
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Anti mitochondrial

4. What are the function of B cells?
Superior mesenteric
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
T
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

5. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Previous transfusion; pregnant woman whose fetus had paternal antigens
Axillary

6. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
T cell activation; no with CD 4 or CD 8
T cell precursor
IL 5

7. what ensure that a memory response is generated?
A j chain
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
If there is class switching and plasma cell production (that is when memory cells are produced)
Anti Jo -1

8. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

9. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
opsonizes

10. What are the autoantibodies for pernicious anemia?
Anti IF
Th cells fail to produce interferon gamma; a lot of IgE
Paracortex; viral infection
Cytokine IL 10 secreted by Th2

11. What does interferon gamma do? What two type of cells does it attack mostly?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Anti Ach receptor

12. What are some catalase positive organisms?
Anti viral and anti tumor
Humoral
S. aureus - E. Coli - aspergillus
Antihistone

13. What are the main symptoms of T cell immunodeficiencies?
T cell dysfunction
No because no peptide fragment!
DM type I
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

14. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Cyclosporine - OKT3
Antibody mediated cytotoxicity; either complement dependent or complement independent
Secretory component

15. What is the main function of IL 12? other than macrophages who else can release IL 12?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Secretory component
Liver! (they are proteins circulating in the blood)

16. What are the two signals required for Th1 cells? what happens after then activated?
DM type I and RA
Antidesmoglein
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

17. which cytokine inhibits TH2 cells? secreted by who?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti Jo -1
Interferon gamma; Th1

18. IgE has the ___________ in the serum
IgM and IgD
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
lowest concentration
delayed!

19. What is the pathogenesis of a hypersensitivity reaction?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Popliteal
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

20. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

21. The lymphocytes are ________ origin
C5a
Basophils! THey want IG E class switch!
dimer
mesenchymal

22. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
dimer
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
MHC II - B7

23. What does IgA pick up from epithelial cells before being secreted?
Secretory component
Increases expression of MHC I and MHC II and also activates NK cells
Macrophages - Dendritic cells - B cells
lowest concentration

24. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Interferon gamma and IL 2
Its a serine protease that activates apoptosis; NK and CD8
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Chronic granulomatous disease

25. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
pathogenesis
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

26. which of the transplant rejections is antibody mediated? why does it occur?
IL 3; supports growth and differentiation of bone marrow stem cells
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
A recomb cytokine of IL 2; RCC and metastatic melanoma
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

27. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Superior mesenteric
Histamine; post capillary venules - vasodilation

28. what cell surface proteins are on all APCs?
MHC II - B7
T cell dysfunction
Th cells fail to produce interferon gamma; a lot of IgE
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

29. Complements are...
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
NK cells
acute phase reactants
Superficial inguinal

30. __________ are a part of the innate system.
dimer
NK cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

31. IgM can exist as a _______ also
pentamer
Active; passive - fast but short half life (3 weeks!)
RNA segment reassortment
Antidesmoglein

32. What are MHC's necessary for? By themselves?
Superficial inguinal
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
T cell activation; no with CD 4 or CD 8
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

33. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Anti smooth muscle
2 heavy chains and two light chains

34. How fast does it occur?
The patient could become cyanotic in the OR!
IgA
S. aureus - E. Coli - aspergillus
Recom IL 11; thrombocytopenia

35. 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?
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
Histamine; post capillary venules - vasodilation
Anti Jo -1
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

36. How does complement link innate and adaptive?
Activate macrophages
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
cannot cross placenta

37. 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
Stimulate the liver to release acute phase reactants
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
CD21 on B cells (although there is T cell lymphocytosis in EBV)

38. What is thrombopoietin used for?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
A chemotactic factor for neutrophils
Lymphocytes
Thrombocytopenia

39. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Severe pyogenic infections early in life

40. What is the main cytokine released by T cells? What does it do
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IL 3; supports growth and differentiation of bone marrow stem cells
Viral neutralization of igM and IgG!
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

41. How is sirolimus different from tacrolimus?
Influenza; antigenic shift; antigenic drift
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

42. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
Axillary
A j chain
Previous transfusion; pregnant woman whose fetus had paternal antigens

43. What is the most common example of passive immunity?
IgAs in mothers breast milk!
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
Liver! (they are proteins circulating in the blood)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

44. What cytokines to Th2 secrete?
Severe pyogenic infections early in life
Alternative splicing of mRNA
IL 4 - 5 - 10 - 6
pale central germinal centers

45. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti topoisomerase
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

46. What do multimeric antibodies require for assembly?
Axillary
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
A j chain

47. Which disease is associated with HLA A3?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Antidote for digoxin intoxication
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Hemochromatosis

48. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
IgM and IgG
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Macrophages - Dendritic cells - B cells

49. can igG cross the placenta?
Yes
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti Jo -1

50. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Anemias (esp due to renal failure)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Severe pyogenic infections early in life