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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.
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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. which of the hypersensitivity reactions is not Ab mediated?
Basophils! THey want IG E class switch!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Type IV

2. what characterizes an arthus reaction?
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
Edema and necrosis in that region
Antidesmoglein
All MHC 1/CD8

3. From where do cytokines come from?
isotype
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
type four
Lymphocytes

4. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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 :(
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

5. What are the autoantibodies for pernicious anemia?
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
Para aortic
Anti IF
Secretory component

6. What are MHC's necessary for? By themselves?
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
Carbohydrate
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
T cell activation; no with CD 4 or CD 8

7. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
MHC I - CD16 - CD56
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

8. What is colostrum?
Activates cytotoxic CD 8 T cells as second signal
The igA found in breast milk
T cell activation; no with CD 4 or CD 8
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

9. In general What are T cells good for?
Anti viral and anti tumor
lowest concentration
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Inferior mesenteric

10. What does IgA pick up from epithelial cells before being secreted?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
Secretory component
Th cells fail to produce interferon gamma; a lot of IgE

11. The lymphocytes are ________ origin
CD21 on B cells (although there is T cell lymphocytosis in EBV)
MHC class molecules bind to KIRS or CD94 to prevent killing
mesenchymal
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

12. What is the treatment of acute transplant rejection?
Interferon gamma and IL 2
Delayed type hypersensitivity
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Cyclosporine - OKT3

13. Type IV hypersensitivity is i...
not Ab mediated
RNA segment reassortment
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Thrombocytopenia

14. 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?
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
Immunosuppression after kidney transplantation
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgA

15. Which MHC presents intracellular peptides? how so?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
T cell activation; no with CD 4 or CD 8
MHC I; from RER with help of the B2 microglobulin

16. What do multimeric antibodies require for assembly?
A j chain
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
not Ab mediated
IgG

17. What are the autoantibodies for drug induced lupus?
B - T - and NK cells
Stimulate the liver to release acute phase reactants
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Antihistone

18. What lymph node drains the duodenum - jejunum?
Negative selection
Superior mesenteric
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

19. What are the two signals required for T cells? what happens after?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
CD21 on B cells (although there is T cell lymphocytosis in EBV)

20. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
A - B - C; all the D's

21. What is Aldesleukin? What is it used for
Anti topoisomerase
A recomb cytokine of IL 2; RCC and metastatic melanoma
Thrombocytopenia
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

22. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
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
Chronic granulomatous disease
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

23. Name 5 ways Antibody diversity is generated?
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
A j chain

24. What lymph node drains the upper limb?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Axillary
except hyperacute
Cyclosporine - OKT3

25. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Superficial inguinal
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
pale central germinal centers
Antihistone

26. 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?
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
If there is class switching and plasma cell production (that is when memory cells are produced)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

27. which antibody is involved in the primary response or immediate response to an antigen?
Basophils! THey want IG E class switch!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Daclizumab; prevent ACUTE rejection of renal transplant
IgM

28. which of the transplant rejections is antibody mediated? why does it occur?
except hyperacute
Active; passive - fast but short half life (3 weeks!)
secondary
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

29. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
DM type I
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
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 :(
Anti smooth muscle

30. How is the antigen loaded onto a MHC II?
Humoral
IgA
Glycoproteins; HLA
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

31. What bugs can actually infect the lymph node itself?
T cell precursor
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
IgE
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

32. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Rheumatic arthritis
Inferior mesenteric
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

33. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
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
Lymphocytes
IgAs in mothers breast milk!

34. What are the autoantibodies for hashimotos?
TGF beta and IL 10
The igA found in breast milk
Antimicrosomal and antithyroglobulin
Increases expression of MHC I and MHC II and also activates NK cells

35. Which type of selection of thymic development provides central tolerance?
encapsulated
Local infection/inflammation; infection of the ln itself; metastasis
Celiac
Negative selection

36. In thymic development - What is the positive selection? negative selections?
Edema and necrosis in that region
Secretory component
When you select for which MHC it will have; take out the lymphs that self react
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

37. The two heavy chains of an antibody contribute to the...
Fab portion
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
S. aureus - E. Coli - aspergillus

38. The Fc region is found on the...
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
carboxy terminal
Humoral
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

39. What are the autoantibodies for goodpastures syndrome?
No because no peptide fragment!
Anti alpha subunit 3 of collagen on type IV bm
S. aureus - E. Coli - aspergillus
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

40. What is chronic mucocutaneous candidiasis d/t?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
T cell dysfunction
Barrel hoop basement membrane fenestrations
A recomb cytokine of IL 2; RCC and metastatic melanoma

41. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
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
Delayed type hypersensitivity

42. What are the main symptoms of B cell immunodeficiencies?
SP infections
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IgG
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

43. what ensure that a memory response is generated?
opsonizes
If there is class switching and plasma cell production (that is when memory cells are produced)
Recom IL 11; thrombocytopenia
Activates Th1 helper cells; Macrophages

44. What are the autoantibodies for systemic sclerosis?
Axillary
Anti topoisomerase
Anti Ach receptor
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

45. Which disease is associated with DR7?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Steroid responsive nephrotic syndrome
SP infections
DM type I and RA

46. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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 :(
Axillary

47. 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
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)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

48. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Liver! (they are proteins circulating in the blood)
2 heavy chains and two light chains
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

49. What is thrombopoietin used for?
Superficial inguinal
Thrombocytopenia
TLR ad nuclear receptors
Edema and necrosis in that region

50. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
Anti alpha subunit 3 of collagen on type IV bm
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Lymphocytes