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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. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
Its a serine protease that activates apoptosis; NK and CD8
Interferon gamma and IL 2
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

2. What are the main symptoms of B cell immunodeficiencies?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
SP infections
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
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

3. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
Acts as second signal on B cells to induce class switching to IgE and IgG
pathogenesis

4. what will NK cells do to cells covered in IgG Ab? why?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Kill them because they have CD16 on them that recognize the FcG portion
Anti U1 RNP (ribonucleoprotein)

5. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
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
Anti glutamate carboxylase and anti insulin
Axillary

6. Give an example of someone who could get hyperacute transplant rejection.
Anti mitochondrial
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgM and IgA
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

7. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Negative selection
DM type I

8. What are the three types of APCs?
Internal iliac
By transcytosis
Activates Th1 helper cells; Macrophages
Macrophages - Dendritic cells - B cells

9. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Celiac
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
...

10. What do multimeric antibodies require for assembly?
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
Antidesmoglein
A j chain
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

11. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Viral neutralization of igM and IgG!
Alternative splicing of mRNA
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

12. Only the _______ contribute to the Fc region
A - B - C; all the D's
heavy chains
Antimicrosomal and antithyroglobulin
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. which of the hypersensitivity reactions is not Ab mediated?
Anti IF
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
Type IV
Kill them because they have CD16 on them that recognize the FcG portion

14. What are some catalase positive organisms?
Anti SS- A (anti RO) and Anti SS- B
In the germinal center of secondary follicles (In the paler center)
IgA
S. aureus - E. Coli - aspergillus

15. Which disease is associated with HLA A3?
Hemochromatosis
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
Anti viral and anti tumor
Remove encapsulated bacateria

16. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Superior mesenteric
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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!

17. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
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

18. What does IL 5 do?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Celiac

19. Type Iv hypersensitivity is...
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
delayed!
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

20. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Tetanus - Botulinum - HBV - Rabies
Anti alpha subunit 3 of collagen on type IV bm

21. The alternative pathway is the only constutively...
mesenchymal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
active complement pathway
Negative selection

22. __________ are a part of the innate system.
NK cells
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
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
Tetanus - Botulinum - HBV - Rabies

23. what mediates the type II hypersensitivity? What are the two different methods?
Glycoproteins; HLA
Antibody mediated cytotoxicity; either complement dependent or complement independent
Tetanus - Botulinum - HBV - Rabies
Interferon gamma; Th1

24. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Th cells fail to produce interferon gamma; a lot of IgE
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
Type IV

25. What lymph node drains the breast?
Axillary
Superficial inguinal
IgE; by activating eosinophils
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

26. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
T cell dysfunction
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
MS

27. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs

28. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
neutrophilia!
acute phase reactants
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

29. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Active; passive - fast but short half life (3 weeks!)
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

30. What are the autoantibodies for systemic sclerosis?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
T
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
Anti topoisomerase

31. What does interferon gamma do? What two type of cells does it attack mostly?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
pathogenesis
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

32. What lymph node drains the thigh?
Superficial inguinal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
The igA found in breast milk
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

33. What does IgA pick up from epithelial cells before being secreted?
Secretory component
dimer
A chemotactic factor for neutrophils
Cyclosporine - OKT3

34. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
TNF alpha and IL1
A chemotactic factor for neutrophils

35. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

36. Type IV hypersensitivity is i...
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
not Ab mediated

37. What is the toxicity of muromonab?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
MHC I; from RER with help of the B2 microglobulin
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Anti viral and anti tumor

38. What are the two signals required for Th1 cells? what happens after then activated?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Graves
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

39. What are the two signals required for B cell class switching? Which is the second signal?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
pentamer
MHC I - CD16 - CD56
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

40. What is epo used for?
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
Anemias (esp due to renal failure)
Antidote for digoxin intoxication
A j chain

41. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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 :(
type four
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

42. give an example of how influenza does a major antigenic shift.
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
Influenza; antigenic shift; antigenic drift
RNA segment reassortment
Interferon gamma; Th1

43. What are the main symptoms of T cell immunodeficiencies?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IL 1 and IL 6
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
TGF beta and IL 10

44. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IgG

45. What is the autoantibody for SLE that is nonspecific? Specific?
pentamer
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

46. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
Its a serine protease that activates apoptosis; NK and CD8
RNA segment reassortment
Immunoflourescent staining of tissue biopsies

47. What is the mechanism for sirolimus? what else it known as?
Its main effect is a defect in Ab opsonization for killing
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

48. What is anergy? why does this occur?
Anti mitochondrial
IL 15; IL 12 - interferon Beta and interferon alpha
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

49. What is the common variable immunodeficiency ? How is it different from Brutons?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Inferior mesenteric
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
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

50. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
T cell activation; no with CD 4 or CD 8
Edema and necrosis in that region
opsonizes