Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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. __________ are a part of the innate system.
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Yes
NK cells
A chemotactic factor for neutrophils

2. Which type of selection of thymic development provides central tolerance?
Negative selection
A j chain
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Paracortex; viral infection

3. What lymph node drains the lateral side of the dorsum of the foot?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Popliteal
type four
Superficial inguinal

4. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
IL 15; IL 12 - interferon Beta and interferon alpha
RNA segment reassortment
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

5. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
Immunosuppression after kidney transplantation
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
CRP - C3b - IgM

6. which antibodies can bind complement?
IgM and IgG
Antibody mediated cytotoxicity; either complement dependent or complement independent
Macrophages - Dendritic cells - B cells
Th cells fail to produce interferon gamma; a lot of IgE

7. Describe complement dependent Type II hypersensitivity. Give an example.
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
T cell precursor
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

8. How is i Th1 helper cell inhibited?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Cytokine IL 10 secreted by Th2
Immunosuppression after kidney transplantation
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

9. What kinds of receptors activate innate immunity?
carboxy terminal
CD56
TLR ad nuclear receptors
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

10. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Rheumatic arthritis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

11. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
Activates cytotoxic CD 8 T cells as second signal
IgG
Anti smooth muscle

12. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Axillary
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

13. what ensure that a memory response is generated?
Paracortex; viral infection
Complement activation (active in both)
If there is class switching and plasma cell production (that is when memory cells are produced)
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

14. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

15. How does complement link innate and adaptive?
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
Liver! (they are proteins circulating in the blood)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

16. What type of fenestrations are found in the red pulp of the spleen?
Chronic granulomatous disease
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Barrel hoop basement membrane fenestrations
Pernicious Anemia and Hashimotos

17. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
IL 4
Anti mitochondrial
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

18. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antidote for digoxin intoxication
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IL 5

19. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Humoral
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

20. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
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
Macrophages - Dendritic cells - B cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

21. What are the two signals required for Th1 cells? what happens after then activated?
Superior mesenteric
Activates cytotoxic CD 8 T cells as second signal
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

22. What are the autoantibodies for Mixed connective tissue disease?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Anti U1 RNP (ribonucleoprotein)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

23. What does it mean if there are igM in the serum at birth?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Activates Th1 helper cells; Macrophages
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

24. which type of immunity is slow but long lasting? as opposed to...
CD56
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
Active; passive - fast but short half life (3 weeks!)

25. which antibody is involved in the primary response or immediate response to an antigen?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
IgM

26. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Type IV
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
T

27. Which helper T cells' development is induced by IL 4? IL 12?
When you select for which MHC it will have; take out the lymphs that self react
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Th2; Th1
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

28. What is the toxicity of azathioprine?
Anti topoisomerase
...
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

29. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Glycoproteins; HLA
Anti Jo -1
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

30. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Th2; Th1
MHC I; from RER with help of the B2 microglobulin
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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

31. can igG cross the placenta?
Negative selection
Steroid responsive nephrotic syndrome
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
Yes

32. Which disease is associated withB B27?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Chronic granulomatous disease
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
B - T - and NK cells

33. What is the presentation of scid? treatment?
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

34. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
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
IL 1 and IL 6
Hemochromatosis

35. IgE has the ___________ in the serum
lowest concentration
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
The igA found in breast milk
Basophils! THey want IG E class switch!

36. what secretes IL 4?
Basophils! THey want IG E class switch!
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
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

37. which antibody activate mast cells - basophils - and eosinophils?
IgE
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

38. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

39. Which diseases are associated with DR2?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
MS - hay fever - SLE - goodpastures
Superficial inguinal

40. What is oprelevkin? and What is it used for?
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
Recom IL 11; thrombocytopenia
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

41. What is the main cytokine that activates eosinophils?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Anti alpha subunit 3 of collagen on type IV bm
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IL 5

42. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
except hyperacute

43. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
MHC class molecules bind to KIRS or CD94 to prevent killing
IgM and IgG
not Ab mediated

44. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
IgM and IgG
Anti topoisomerase
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Thrombocytopenia

45. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
TLR ad nuclear receptors
Complement activation (active in both)
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

46. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Antimicrosomal and antithyroglobulin
Hereditary angioedema; PNH
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Local infection/inflammation; infection of the ln itself; metastasis

47. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Negative!
2 heavy chains and two light chains
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

48. What is three common causes of severe combined immunodef? What is the result of all three?
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!
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgM
IL 3; supports growth and differentiation of bone marrow stem cells

49. What are the PALS?
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
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

50. where do somatic hypermutation and class switching occur?
Anti mitochondrial
In the germinal center of secondary follicles (In the paler center)
Histamine; post capillary venules - vasodilation
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction