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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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1. what ensure that a memory response is generated?
IL 4 - 5 - 10 - 6
In the germinal center of secondary follicles (In the paler center)
If there is class switching and plasma cell production (that is when memory cells are produced)
IgG

2. What is Aldesleukin? What is it used for
cannot cross placenta
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
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

3. 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
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
T cell activation; no with CD 4 or CD 8
pathogenesis

4. What are the autoantibodies for drug induced lupus?
Antihistone
Axillary
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Anti topoisomerase

5. What is the pathology of acute transplant rejection? is it reversible?
False! B cell class switching requires a second signal
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 3; supports growth and differentiation of bone marrow stem cells
Cytokine IL 10 secreted by Th2

6. What lymph node drains the upper limb?
Axillary
IgG
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

7. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Immunoflourescent staining of tissue biopsies

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

9. What are the autoantibodies for autoimmune hepatitis?
Immunosuppression after kidney transplantation
Anti smooth muscle
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

10. What is the autoantibody for SLE that is nonspecific? Specific?
Hereditary angioedema; PNH
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Cyclosporine - OKT3

11. How is the thymus organized? what happens in each section?
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
Its a serine protease that activates apoptosis; NK and CD8
CD56
Its main effect is a defect in Ab opsonization for killing

12. What are superantigens? give two examples.
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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

13. what cell surface proteins are on all APCs?
...
MHC II - B7
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgM

14. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
Paracortex; viral infection
A recomb cytokine of IL 2; RCC and metastatic melanoma
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

15. What are the autoantibodies for hashimotos?
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
Influenza; antigenic shift; antigenic drift
T cell activation; no with CD 4 or CD 8
Antimicrosomal and antithyroglobulin

16. What are the two signals required for T cells? what happens after?
Stimulate the liver to release acute phase reactants
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Anti U1 RNP (ribonucleoprotein)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

17. What are the autoantibodies for graves?
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
Anti TSh receptor
Antihistone
Anti SS- A (anti RO) and Anti SS- B

18. What is the treatment of acute transplant rejection?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Cyclosporine - OKT3
neutrophilia!

19. can igG cross the placenta?
secondary
Yes
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

20. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
Carbohydrate
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

21. What are the major functions of Antibodies?
DM type I and RA
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (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
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

22. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Th cells fail to produce interferon gamma; a lot of IgE
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

23. which antibodies can bind complement?
IgM and IgG
Inferior mesenteric
Edema and necrosis in that region
Bind FcG for antibody dependent cellular cytotoxicity

24. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
delayed!
A - B - C; all the D's
Celiac

25. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
T cell activation; no with CD 4 or CD 8
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
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

26. The secondary follicles have __________; primary follicles are dense
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
False! B cell class switching requires a second signal
pale central germinal centers
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

27. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
IgE; by activating eosinophils
Steroid responsive nephrotic syndrome
Liver! (they are proteins circulating in the blood)
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

28. What are target cells?
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!
heavy chains
Cells that stil have weird parts of their membrane that macrophages usually bite off
False! B cell class switching requires a second signal

29. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
active complement pathway
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

30. 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)?
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 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
Cytokine IL 10 secreted by Th2
RNA segment reassortment

31. The alternative pathway is the only constutively...
Edema and necrosis in that region
Th2; Th1
Influenza; antigenic shift; antigenic drift
active complement pathway

32. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

33. What are C1 - C2 - C3 - C4 important for?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Cells that stil have weird parts of their membrane that macrophages usually bite off
encapsulated
Viral neutralization of igM and IgG!

34. What are the T cell functions?
NK cells
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

35. From where do cytokines come from?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Negative!
Lymphocytes
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

36. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
Graves
NK cells

37. What are the two signals to kill for NK cells?
Delayed type hypersensitivity
Severe pyogenic infections early in life
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IL 1 and IL 6

38. How is the antigen loaded onto a MHC II?
A chemotactic factor for neutrophils
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
Anti alpha subunit 3 of collagen on type IV bm

39. Which are the only two antiinflammatory cytokines?
By transcytosis
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
TGF beta and IL 10
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

40. What are the autoantibodies for pernicious anemia?
Anti IF
Cytokine IL 10 secreted by Th2
Alternative splicing of mRNA
Interferon gamma and IL 2

41. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Th cells fail to produce interferon gamma; a lot of IgE
Anti SS- A (anti RO) and Anti SS- B
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
Interferon gamma; Th1

42. Type IV hypersensitivity is i...
not Ab mediated
Activate macrophages
Anti smooth muscle
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

43. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Lymphocytes
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
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

44. What is the clinical use of Muromonab?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
dimer
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
Immunosuppression after kidney transplantation

45. What is the main cytokine released by T cells? What does it do
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
S. aureus - E. Coli - aspergillus
Alternative splicing of mRNA
IL 3; supports growth and differentiation of bone marrow stem cells

46. What does granzyme do? who secretes it?
Negative nitroblue tetrazolium reduction test
Superficial inguinal
Barrel hoop basement membrane fenestrations
Its a serine protease that activates apoptosis; NK and CD8

47. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Active; passive - fast but short half life (3 weeks!)
IgG
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

48. What is the pathogenesis of a hypersensitivity reaction?
IgM and IgA
Severe pyogenic infections early in life
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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

49. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Anti IF
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
C5a

50. What are the autoantibodies for pemphigus bulgaris?
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
Antidesmoglein
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Cells that stil have weird parts of their membrane that macrophages usually bite off