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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 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
Antihistone
pale central germinal centers
...

2. Which is the most abundant antibody in blood?
S. aureus - E. Coli - aspergillus
Delayed type hypersensitivity
In the germinal center of secondary follicles (In the paler center)
IgG

3. Which MHC presents intracellular peptides? how so?
MHC I; from RER with help of the B2 microglobulin
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Superior mesenteric
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

4. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Celiac
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
A recomb cytokine of IL 2; RCC and metastatic melanoma
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

5. What is the most common selective Ig deficiency? What is the presentation?
secondary
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
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

6. Which disease is associated with DR7?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Steroid responsive nephrotic syndrome
Fc
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

7. what cytokine does basophils secrete?
IL 4
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
In the germinal center of secondary follicles (In the paler center)
lowest concentration

8. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Remove encapsulated bacateria
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgG
pale central germinal centers

9. What is the clinical use for azathioprine?
IgM and IgA
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
...

10. Give three examples of bacteria that use antigenic variation and how.
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 in combination with cyclosporine and corticosteroids
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

11. What lymph node drains the sigmoid colon?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Acts as second signal on B cells to induce class switching to IgE and IgG
Inferior mesenteric

12. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
If there is class switching and plasma cell production (that is when memory cells are produced)
Daclizumab; prevent ACUTE rejection of renal transplant
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

13. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
Basophils! THey want IG E class switch!
Lymphocytes
Interferon gamma and IL 2

14. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC I; from RER with help of the B2 microglobulin
Th cells fail to produce interferon gamma; a lot of IgE
Previous transfusion; pregnant woman whose fetus had paternal antigens

15. What are the autoantibodies for other vasculitides?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Tetanus - Botulinum - HBV - Rabies
active complement pathway
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

16. What lymph node drains the anal canal (below the pectinate line)?
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
Superficial inguinal
Th2; Th1
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

17. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Delayed type hypersensitivity
By transcytosis
Its main effect is a defect in Ab opsonization for killing
isotype

18. What is the receptor for EBV? On what cells is that located?
Kill them because they have CD16 on them that recognize the FcG portion
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Secretory component
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

19. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
When you select for which MHC it will have; take out the lymphs that self react
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
T cell precursor
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

20. where do NK cells develop?
Not thymus - BM
Anti alpha subunit 3 of collagen on type IV bm
IgE
Type IV

21. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Stimulate the liver to release acute phase reactants
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Axillary
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

22. What are the autoantibodies for drug induced lupus?
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
Antihistone
Tetanus - Botulinum - HBV - Rabies
Pernicious Anemia and Hashimotos

23. What is an example of a parasite showing antigenic variation?
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
Active; passive - fast but short half life (3 weeks!)
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 :(
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

24. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Anti glutamate carboxylase and anti insulin
Wiskott Aldrich syndrome
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 antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

25. __________ are a part of the innate system.
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
Activates Th1 helper cells; Macrophages
NK cells
Receiving preformed Antibodies

26. What are the autoantibodies for goodpastures syndrome?
MS
TGF beta and IL 10
Hereditary angioedema; PNH
Anti alpha subunit 3 of collagen on type IV bm

27. What is the white pulp of the spleen?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Sinusitis - otitis media - pneumonia
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

28. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
IgE
Antidote for digoxin intoxication
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

29. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
IgA
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
pathogenesis
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

30. What are the autoantibodies for Celiac disease?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Macrophages - Dendritic cells - B cells

31. What is anergy? why does this occur?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
T
IL 3; supports growth and differentiation of bone marrow stem cells

32. What are the two signals to kill for NK cells?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

33. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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)

34. What is the toxicity of azathioprine?
...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgG
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!

35. Which antibodies can be multimeric?
IgM and IgA
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Recom IL 11; thrombocytopenia

36. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
MS - hay fever - SLE - goodpastures
IgG

37. which antibody activate mast cells - basophils - and eosinophils?
active complement pathway
Negative!
IgE
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

38. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Axillary
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
...
T cell activation; no with CD 4 or CD 8

39. What are the two signals required for B cell class switching? Which is the second signal?
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 :(
Not thymus - BM
Type IV
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

40. which type of immunity is slow but long lasting? as opposed to...
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
False! B cell class switching requires a second signal
Active; passive - fast but short half life (3 weeks!)
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

41. what prevents NK cells from killing normal cells if their default is to kill?
T cell activation; no with CD 4 or CD 8
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 class molecules bind to KIRS or CD94 to prevent killing
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

42. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
TLR ad nuclear receptors
Severe pyogenic infections early in life
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

43. where are complements produced?
except hyperacute
Liver! (they are proteins circulating in the blood)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

44. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
type four

45. Which is the main antibody in the delayed or secondary response to an antigen?
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
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
IgG
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

46. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
IgE
Inferior mesenteric
False! B cell class switching requires a second signal

47. what cell surface proteins are on all APCs?
Anti viral and anti tumor
Anti IF
MHC II - B7
T cell dysfunction

48. describe the classic complement pathway.
Humoral
In the germinal center of secondary follicles (In the paler center)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

49. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

50. IgE has the ___________ in the serum
lowest concentration
IgE; by activating eosinophils
IL 4 - 5 - 10 - 6
pentamer