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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 autoantibody for SLE that is nonspecific? Specific?
pathogenesis
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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

2. What are the main symptoms of T cell immunodeficiencies?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

3. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Antidesmoglein
Anti viral and anti tumor
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Superficial inguinal

4. what cell surface proteins are on all APCs?
MHC II - B7
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Cytokine IL 10 secreted by Th2
Hemochromatosis

5. What lymph node drains the sigmoid colon?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anti smooth muscle
Inferior mesenteric
Anti IF

6. What are the autoantibodies for Celiac disease?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

7. Which MHC presents intracellular peptides? how so?
T cell dysfunction
...
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
MHC I; from RER with help of the B2 microglobulin

8. What are the major functions of Antibodies?
The igA found in breast milk
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Para aortic
MHC I - CD16 - CD56

9. what happens in a deficiency of C1 esterase inhibitor? DAF?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Hereditary angioedema; PNH
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

10. What are the autoantibodies for type I diabetes mellitus?
TLR ad nuclear receptors
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anti glutamate carboxylase and anti insulin
Tetanus - Botulinum - HBV - Rabies

11. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
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
All MHC 1/CD8
IgM and IgG
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

12. The two heavy chains of an antibody contribute to the...
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
Fab portion
TLR ad nuclear receptors
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

13. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
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!
Negative!
Influenza; antigenic shift; antigenic drift
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

14. What lymph node drains the rectum (above the pectinate line)?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Internal iliac
isotype
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

15. What is Aldesleukin? What is it used for
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Inferior mesenteric
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
A recomb cytokine of IL 2; RCC and metastatic melanoma

16. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Anti TSh receptor
IgE
Daclizumab; prevent ACUTE rejection of renal transplant
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

17. __________ are a part of the innate system.
NK cells
Superior mesenteric
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!)

18. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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
Glycoproteins; HLA

19. Leukocyte adhesion defect presents with...
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
except hyperacute
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
neutrophilia!

20. How does the alternative pathway lead to MAC activation?
Superficial inguinal
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

21. From where do cytokines come from?
Lymphocytes
IL 3; supports growth and differentiation of bone marrow stem cells
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IgM

22. IgG...
opsonizes
Activate macrophages
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

23. What is the clinical use for azathioprine?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

24. What is the most common example of passive immunity?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Chronic granulomatous disease
IgAs in mothers breast milk!
acute phase reactants

25. which interleukin receptor is required for NK development? activation?
CRP - C3b - IgM
IL 15; IL 12 - interferon Beta and interferon alpha
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Its a serine protease that activates apoptosis; NK and CD8

26. What do mature naive B lymphocytes express?
IgM and IgD
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
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
Popliteal

27. What are the main symptoms of B cell immunodeficiencies?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
SP infections
Complement activation (active in both)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

28. What is the clinical use of Muromonab?
False! B cell class switching requires a second signal
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Immunosuppression after kidney transplantation

29. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
encapsulated
Th2; Th1
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
except hyperacute

30. Name 5 ways Antibody diversity is generated?
Paracortex
Anti topoisomerase
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
Paracortex; viral infection

31. What is the presentation of scid? treatment?
mesenchymal
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
Anti SS- A (anti RO) and Anti SS- B

32. 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?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
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

33. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Kill them because they have CD16 on them that recognize the FcG portion
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

34. Other than stimulating fever - what else does IL 6 do?
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
Stimulate the liver to release acute phase reactants
C5a
Barrel hoop basement membrane fenestrations

35. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
except hyperacute
Complement activation (active in both)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

36. What are the cell surface proteins on NK cells?
Anti IF
Negative nitroblue tetrazolium reduction test
MHC I - CD16 - CD56
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

37. which cells have more complete tolerance - B or T cells?
T
T cell dysfunction
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
CD56

38. What are the autoantibodies for other vasculitides?
MHC I - CD16 - CD56
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
Paracortex; viral infection

39. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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
Delayed type hypersensitivity
Alternative splicing of mRNA
Type IV

40. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Anti SS- A (anti RO) and Anti SS- B
Activate macrophages
mesenchymal

41. What is thrombopoietin used for?
Receiving preformed Antibodies
Pernicious Anemia and Hashimotos
delayed!
Thrombocytopenia

42. What can cause a lymph node enlargement?
Influenza; antigenic shift; antigenic drift
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Local infection/inflammation; infection of the ln itself; metastasis
isotype

43. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Hemochromatosis
Rheumatic arthritis
Anti U1 RNP (ribonucleoprotein)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

44. What type of side chains are found on Fc region of an antibody?
Carbohydrate
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antidesmoglein

45. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
By transcytosis
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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

46. In general What are T cells good for?
Anti viral and anti tumor
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
No because no peptide fragment!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

47. What is recomb gamma interferon used for?
Anti SS- A (anti RO) and Anti SS- B
Chronic granulomatous disease
Negative nitroblue tetrazolium reduction test
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

48. 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).
Activate macrophages
T cell activation; no with CD 4 or CD 8
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!
Cytokine IL 10 secreted by Th2

49. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Increases expression of MHC I and MHC II and also activates NK cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
MS

50. What is the late phase reaction of anaphylaxis allergy? what mediates it?
In the germinal center of secondary follicles (In the paler center)
Not thymus - BM
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
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)