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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. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Paracortex; viral infection
Axillary

2. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Inferior mesenteric
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

3. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
MHC II - B7
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
A recomb cytokine of IL 2; RCC and metastatic melanoma
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

4. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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
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

5. What lymph node drains the lateral side of the dorsum of the foot?
Glycoproteins; HLA
Para aortic
Popliteal
Superficial inguinal

6. What is thrombopoietin used for?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Thrombocytopenia

7. What is passive immunity?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Receiving preformed Antibodies
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

8. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
neutrophilia!
pentamer

9. what will NK cells do to cells covered in IgG Ab? why?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Kill them because they have CD16 on them that recognize the FcG portion
Tetanus - Botulinum - HBV - Rabies
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

10. What are the autoantibodies for Mixed connective tissue disease?
cannot cross placenta
Chronic granulomatous disease
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti U1 RNP (ribonucleoprotein)

11. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Anti U1 RNP (ribonucleoprotein)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
pentamer

12. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
If there is class switching and plasma cell production (that is when memory cells are produced)
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

13. What are the cell surface proteins on NK cells?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
MHC I - CD16 - CD56
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
Wiskott Aldrich syndrome

14. What are the autoantibodies for pemphigus bulgaris?
B - T - and NK cells
Antidesmoglein
A j chain
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!

15. what characterizes an arthus reaction?
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
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
Edema and necrosis in that region
Th2; Th1

16. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

17. ________ regulate the cell mediated response.
Cells that stil have weird parts of their membrane that macrophages usually bite off
Humoral
...
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

18. What portion of the lymph node is not well developed in DiGeorge Syndrome?
pale central germinal centers
Graves
Severe pyogenic infections early in life
Paracortex

19. What are the autoantibodies for pernicious anemia?
B - T - and NK cells
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
Anti IF
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

20. How is i Th1 helper cell inhibited?
Anti mitochondrial
Cytokine IL 10 secreted by Th2
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

21. What does granzyme do? who secretes it?
Hereditary angioedema; PNH
IL 3; supports growth and differentiation of bone marrow stem cells
T cell precursor
Its a serine protease that activates apoptosis; NK and CD8

22. What are the cell surface proteins for Macrophages? which two are for opsonins?
...
Anti glutamate carboxylase and anti insulin
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

23. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Cyclosporine - OKT3
Glycoproteins; HLA
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

24. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
Lymphocytes
Activates cytotoxic CD 8 T cells as second signal
Activate macrophages

25. What lymph node drains the scrotum?
Yes
Hereditary angioedema; PNH
T
Superficial inguinal

26. What are the labs in brutons agammaglobulinemia?
B - T - and NK cells
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
...
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

27. what prevents NK cells from killing normal cells if their default is to kill?
Inferior mesenteric
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MHC class molecules bind to KIRS or CD94 to prevent killing
Pernicious Anemia and Hashimotos

28. What lymph node drains the breast?
Antidesmoglein
Macrophages - Dendritic cells - B cells
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Axillary

29. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Delayed type hypersensitivity
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

30. What are the T cell functions?
IL 15; IL 12 - interferon Beta and interferon alpha
Popliteal
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

31. IgG...
opsonizes
No because no peptide fragment!
Humoral
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

32. What type of side chains are found on Fc region of an antibody?
Anti Jo -1
Its main effect is a defect in Ab opsonization for killing
Carbohydrate
Anti topoisomerase

33. What happens in a deficiency of C3?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Kill them because they have CD16 on them that recognize the FcG portion

34. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

35. Which HLA's are included in MHC I? MHC II?

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36. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

37. What lymph node drains the duodenum - jejunum?
not Ab mediated
A chemotactic factor for neutrophils
Superior mesenteric
Anti viral and anti tumor

38. How does the alternative pathway lead to MAC activation?
Acts as second signal on B cells to induce class switching to IgE and IgG
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
Negative!
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

39. What is the most common selective Ig deficiency? What is the presentation?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

40. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Rheumatic arthritis
The igA found in breast milk
Carbohydrate

41. What is the main cytokine that activates eosinophils?
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
IL 5
False! B cell class switching requires a second signal
Activates cytotoxic CD 8 T cells as second signal

42. What is the white pulp of the spleen?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Rheumatic arthritis
CRP - C3b - IgM

43. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Immunoflourescent staining of tissue biopsies

44. What is epo used for?
Th cells fail to produce interferon gamma; a lot of IgE
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Activate macrophages
Anemias (esp due to renal failure)

45. What bugs can actually infect the lymph node itself?
neutrophilia!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

46. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Local infection/inflammation; infection of the ln itself; metastasis

47. What are some sinopulmonary infections?
Cross link
Cells that stil have weird parts of their membrane that macrophages usually bite off
Sinusitis - otitis media - pneumonia
Interferon gamma; Th1

48. What are the three types of lymphocytes?
CRP - C3b - IgM
IL 3; supports growth and differentiation of bone marrow stem cells
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
B - T - and NK cells

49. Complements are...
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Activates cytotoxic CD 8 T cells as second signal
acute phase reactants

50. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
acute phase reactants
IgA