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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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1. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
Pernicious Anemia and Hashimotos
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Not thymus - BM

2. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
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
Edema and necrosis in that region
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

3. What are the three types of lymphocytes?
Fab portion
Anti IF
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
B - T - and NK cells

4. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Influenza; antigenic shift; antigenic drift
S. aureus - E. Coli - aspergillus
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

5. What is the pathogenesis of a candida skin test?
The patient could become cyanotic in the OR!
IgG
Delayed type hypersensitivity
Secretory component

6. What is the autoantibody for SLE that is nonspecific? Specific?
A - B - C; all the D's
IL 3; supports growth and differentiation of bone marrow stem cells
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

7. What are the symptoms of serum sickness?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
False! B cell class switching requires a second signal
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

8. In general What are T cells good for?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti viral and anti tumor
Negative nitroblue tetrazolium reduction test

9. What is digoxin immune Fab used for?
MHC I - CD16 - CD56
Antidote for digoxin intoxication
Lymphocytes
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

10. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
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 :(
Th cells fail to produce interferon gamma; a lot of IgE
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

11. 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?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

12. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Severe pyogenic infections early in life
Anti TSh receptor
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

13. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
If there is class switching and plasma cell production (that is when memory cells are produced)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

14. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Paracortex; viral infection
The patient could become cyanotic in the OR!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

15. 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?
TGF beta and IL 10
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
The patient could become cyanotic in the OR!

16. Which diseases are associated with DR4?
Activate macrophages
DM type I and RA
Anti Jo -1
MS

17. What are the two signals to kill for NK cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

18. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
except hyperacute
Glycoproteins; HLA
TNF alpha and IL1

19. What is hereditary angioedema? What are the C3 levels?
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
MS - hay fever - SLE - goodpastures

20. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
heavy chains
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IL 3; supports growth and differentiation of bone marrow stem cells

21. What is Aldesleukin? What is it used for
Tetanus - Botulinum - HBV - Rabies
A recomb cytokine of IL 2; RCC and metastatic melanoma
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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

22. What is an example of a parasite showing antigenic variation?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
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

23. Name 5 ways Antibody diversity is generated?
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
Local infection/inflammation; infection of the ln itself; metastasis
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

24. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Activate macrophages
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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

25. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
TLR ad nuclear receptors
mesenchymal
Celiac
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

26. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
delayed!
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

27. when can graft versus host disease? What is the result?
Wiskott Aldrich syndrome
delayed!
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
Negative selection

28. What are the T cell functions?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

29. What are the autoantibodies for sjorgens syndrome?
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
T cell dysfunction
Anti SS- A (anti RO) and Anti SS- B
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

30. What lymph node drains the testes?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Th cells fail to produce interferon gamma; a lot of IgE
Hereditary angioedema; PNH
Para aortic

31. Which is the main antibody in the delayed or secondary response to an antigen?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgG
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

32. __________ are a part of the innate system.
IgG
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
NK cells
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

33. What is the main function of IL 8?
A chemotactic factor for neutrophils
In the germinal center of secondary follicles (In the paler center)
Celiac
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

34. What is the clinical use of Muromonab?
DM type I and RA
Celiac
mesenchymal
Immunosuppression after kidney transplantation

35. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
Daclizumab; prevent ACUTE rejection of renal transplant
Interferon gamma; Th1
IgE; by activating eosinophils

36. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Its main effect is a defect in Ab opsonization for killing
type four
Th cells fail to produce interferon gamma; a lot of IgE
Daclizumab; prevent ACUTE rejection of renal transplant

37. What cytokines to Th2 secrete?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Severe pyogenic infections early in life
Superficial inguinal
IL 4 - 5 - 10 - 6

38. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Its a serine protease that activates apoptosis; NK and CD8
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

39. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Pernicious Anemia and Hashimotos
Steroid responsive nephrotic syndrome
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
T cell activation; no with CD 4 or CD 8

40. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
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)
SP infections
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

41. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
No because no peptide fragment!
MHC I - CD16 - CD56
2 heavy chains and two light chains

42. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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 :(
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
B - T - and NK 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

43. 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
Rheumatic arthritis
Antimicrosomal and antithyroglobulin
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

44. What is the clinical use for azathioprine?
Severe pyogenic infections early in life
...
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

45. what secretes IL 4?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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
Basophils! THey want IG E class switch!
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

46. which type of immunity is slow but long lasting? as opposed to...
Liver! (they are proteins circulating in the blood)
IgG
Active; passive - fast but short half life (3 weeks!)
Immunoflourescent staining of tissue biopsies

47. What is a type I hypersensitivity reaction? What is atopic?
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
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

48. What are the two signals required for B cell class switching? Which is the second signal?
Anti viral and anti tumor
Antihistone
Viral neutralization of igM and IgG!
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

49. What are target cells?
secondary
Axillary
Anemias (esp due to renal failure)
Cells that stil have weird parts of their membrane that macrophages usually bite off

50. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
IgM and IgA
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
Influenza; antigenic shift; antigenic drift
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

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