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USMLE 1 > Immunology- Immune responses > Flashcards

Immunology- Immune responses Flashcards

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1
Q

Antibody structure

and function

A

Fab (containing the variable/hypervariable regions) consisting of light (L) and heavy (H) chains
recognizes antigens.

Fc region of IgM and IgG fixes complement. Heavy chain contributes to Fc and Fab regions. Light chain contributes only to Fab region.

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2
Q

Generation of antibody diversity (antigen

independent)

A
  1. Random recombination of VJ (light-chain)
    or V(D)J (heavy-chain) genes.
  2. Random addition of nucleotides to
    DNA during recombination by terminal
    deoxynucleotidyl transferase (TdT).
  3. Random combination of heavy chains with
    light chains.
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3
Q

Generation of antibody specificity (antigen

dependent)

A
  1. Somatic hypermutation and affinity
    maturation (variable region).
  2. Isotype switching (constant region).
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4
Q

Mature, naive B cells prior to activation express…

A

IgM and IgD

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5
Q

IgG

A

Fixes complement, opsonizes bacteria, neutralizes bacterial toxins and viruses. Only isotype that crosses the placenta

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6
Q

IgA

A

Prevents attachment of bacteria and viruses to mucous membranes; does not fix complement.

Monomer (in circulation) or dimer (with J chain when secreted).

Released into secretions (tears, saliva, mucus) and breast milk.

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7
Q

IgM

A

Antigen receptor on the surface of B cells. Monomer on B cell, pentamer with J chain when secreted.

Pentamer enables avid binding to antigen while humoral response evolves.

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8
Q

IgD

A

Unclear function. Found on surface of many B cells and in serum.

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9
Q

IgE

A

Binds mast cells and basophils; cross-links when exposed to allergen, mediating immediate (type I)
hypersensitivity

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10
Q

Thymus-independent

antigens

A

Antigens lacking a peptide component (eg, lipopolysaccharides from gram ⊝ bacteria); cannot
be presented by MHC to T cells. Weakly immunogenic

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11
Q

Complement activation pathways

A

Classic—IgG or IgM mediated.
Alternative—microbe surface molecules.
Lectin—mannose or other sugars on microbe
surface

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12
Q

Complement function

A

C3b—opsonization.
C3a, C4a, C5a—anaphylaxis.
C5a—neutrophil chemotaxis.
C5b-9—cytolysis by MAC

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13
Q

Complement inhibitors

A

Inhibitors—decay-accelerating factor (DAF, aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells (eg, RBCs).

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14
Q

Early complement deficiencies (C1-C4)

A

Increased risk of severe, recurrent pyogenic sinus and respiratory tract infections. Increased risk of SLE.

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15
Q

Terminal complement deficiencies (C5–C9)

A

Increased susceptibility to recurrent Neisseria bacteremia.

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16
Q

C1 esterase inhibitor

deficiency

A

Hereditary angioedema due to unregulated activation of kallikrein..

Characterized by Lower C4 levels. ACE inhibitors are contraindicated.

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17
Q

Paroxysmal nocturnal

hemoglobinuria

A

PIGA gene preventing the formation of anchors for complement inhibitors, such as (DAF/CD55) and (MIRL/CD59).

Causes complement-mediated lysis of RBCs.

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18
Q

Important cytokines

IL1, 2, 3, 4, 5, 6

A 
“Hot T-bone stEAK”:
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein
production.
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19
Q 
Important cytokines
Il-8
IL-12
INF gamma
IL-10
A

Major chemotactic factor for neutrophils

Induces differentiation of T cells into Th1 cells.

stimulates macrophages to kill phagocytosed pathogens.

Attenuates inflammatory response. Decreases
expression of MHC class II and Th1 cytokines.
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20
Q

Respiratory burst

oxidative burst

A
  1. NADPH oxidase (deficiency = chronic granulomatous disease).
  2. Superoxide dismutase
  3. Myeloperoxidase
  4. Glutathione peroxidase (requires selenium)
  5. Glutathione reductase (requires riboflavin)
  6. G6PD
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21
Q

Pyocianin

A

of P aeruginosa generates ROS to kill competing pathogens.

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22
Q

Lactoferrin

A

is a protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation.

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23
Q

Interferon-α and -β

Study These Flashcards
A

A part of innate host defense against both RNA and DNA viruses. Are glycoproteins synthesized by virus-infected cells.

24
Q 
Cell surface proteins
T cells 
- Helper t cells
- Cytotoxic T cells 
- Regulatory T cells
Study These Flashcards
A

TCR (binds antigen-MHC complex)
CD3 (associated with TCR for signal transduction)
CD28 (binds B7 on APC)

  • Helper T cells CD4, CD40L, CXCR4/CCR5 (co-receptor for HIV)
  • CD8
  • CD4, CD25
25
Cell surface proteins | B cells
Ig (binds antigen) CD19, CD20, CD21 (receptor for EBV), CD40 MHC II, B7
26
Cell surface proteins | Macrophages
CD14 (receptor for PAMPs, eg, LPS), CD40 CCR5 MHC II, B7 (CD80/86) Fc and C3b receptors (enhanced phagocytosis)
27
Cell surface proteins | NK
CD16, CD56 (suggestive marker for NK)
28
Cell surface proteins | Hematopoietic stem cells
CD34
29
After exposure to... unvaccinated patients are given preformed antibodies (passive immunity).
"To Be Healed Very Rapidly” Tetanus toxin, Botulinum toxin, HBV, Varicella, Rabies virus, or diphtheria toxin.
30
Live attenuated vaccine | cellular and humoral responses
“Attention! Please Vaccinate Small, Beautiful Young Infants with MMR Regularly!” Adenovirus (nonattenuated, given to military recruits), Polio (sabin), Varicella (chickenpox), Smallpox, BCG, Yellow fever, Influenza (intranasal), MMR, Rotavirus.
31
Killed or inactivated vaccine | humoral responses
SalK = Kille RIP Always Rabies, Influenza (injection), Polio (Salk), hepatitis A.
32
Subunit vaccine (only the antigens that best stimulate the immune system)
``` HBV (antigen = HBsAg), HPV (types 6, 11, 16, and 18), acellular pertussis (aP), Neisseria meningitidis (various strains), Streptococcus pneumoniae Haemophilus influenzae type b. ```
33
Toxoid vaccine | Denatured bacterial toxin
Denatured bacterial toxin
34
Hypersensitivity types
``` (ABCD): Anaphylactic and Atopic (type I), antiBody-mediated (type II), Immune Complex (type III), Delayed (cell-mediated, type IV). ```
35
Direct Coombs test Indirect Coombs test
detects antibodies attached directly to the RBC surface. detects presence of unbound antibodies in the serum
36
Serum sickness—
the prototype immune complex disease. Antibodies to foreign proteins are produced and 1–2 weeks later, antibodyantigen complexes form and deposit in tissues, complement activation, inflammation and tissue damage.
37
Arthus reaction
A local subacute immune complex-mediated hypersensitivity reaction. Intradermal injection of antigen into a presensitized individual leads to immune complex formation in the skin.
38
IV hypersensitivity
4T’s: T cells, Transplant rejections, TB skin tests, Touching (contact dermatitis). Fourth (type) and last (delayed).
39
Blood transfusion reactions
Allergic/anaphylactic reaction. Febrile nonhemolytic transfusion reaction Acute hemolytic transfusion reaction Transfusion-related acute lung injury
40
Autoantibodies
pag. 115 usmle first aid
41
X-linked (Bruton) agammaglobulinemia Defect presentation finding
Defect in BTK,no B-cell maturation. X-linked recessive. Recurrent bacterial and enteroviral infections after 6 months. Absent B cells in peripheral blood, low Ig of all classes. Absent/scanty lymph nodes and tonsils.
42
Selective IgA deficiency Defect presentation finding
Cause Unknown. Most common 1° immunodeficiency. majority Asymptomatic. can see Airway and GI infections, Autoimmune disease, Atopy, Anaphylaxis to IgA-containing products. low IgA with normal IgG, IgM levels
43
Common variable immunodeficiency Defect presentation finding
Defect in B-cell differentiation. Cause is unknown. Presents after age 2 and may be considerably delayed; Risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infections. Low plasma cells, low immunoglobulins.
44
IL-12 receptor deficiency Defect presentation finding
low Th1 response. Autosomal recessive. Disseminated mycobacterial and fungal infections. Low INF gamma
45
Autosomal dominant hyper-IgE syndrome (Job syndrome) Defect presentation finding
Deficiency of Th17 cells due to STAT3 mutation. ``` FATED: coarse Facies, cold (noninflamed) staphylococcal Abscesses, retained primary Teeth, high IgE, Dermatologic problems (eczema). Bone fracture ```
46
Chronic mucocutaneous candidiasis Defect presentation finding
T-cell dysfunction. Can result from congenital genetic defects in IL-17 or IL-17 receptors. Noninvasive Candida albicans infections of skin and mucous membranes. Absent in vitro T-cell proliferation in response to Candida antigens. Absent cutaneous reaction to Candida antigens.
47
Severe combined immunodeficiency Defect presentation finding
Defective IL-2R gamma chain (most common, X-linked recessive), adenosine deaminase deficiency (autosomal recessive). Failure to thrive, chronic diarrhea, thrush. Recurrent viral, bacterial, fungal, and protozoal infections. Absence of thymic shadow (CXR), germinal centers (lymph node biopsy), and T cells (flow cytometry).
48
Ataxia-telangiectasia Defect presentation finding
Defects in ATM gene, failure to detect DNA damage. AR. Triad: cerebellar defects (Ataxia), spider Angiomas (telangiectasia A ), IgA deficiency. high AFP. low IgA, IgG, and IgE. Lymphopenia, cerebellar atrophy.
49
Hyper-IgM syndrome Defect presentation finding
Most commonly due to defective CD40L on Th cells, class switching defect. XR Severe pyogenic infections early in life; opportunistic infection Pneumocystis, Cryptosporidium, CMV. Normal or high IgM. low IgG, IgA, IgE.
50
Wiskott-Aldrich syndrome Defect presentation finding
Mutation in WASp gene; leukocytes and platelets unable to reorganize actin cytoskeleton. XR WATER: Wiskott-Aldrich: Thrombocytopenia, Eczema, Recurrent (pyogenic) infections. low to normal IgG, IgM. High IgE, IgA. Fewer and smaller platelets.
51
Leukocyte adhesion deficiency (type 1) Defect presentation finding
Defect in LFA-1 integrin (CD18) protein on phagocytes; impaired migration and chemotaxis. AR Recurrent skin and mucosal bacterial infections, absent pus, impaired wound healing, delayed (> 30 days) separation of umbilical cord. high neutrophils in blood. Absence of neutrophils at infection sites.
52
Chédiak-Higashi syndrome Defect presentation finding
Defect in lysosomal trafficking regulator gene (LYST). AR PLAIN: Progressive neurodegeneration, Lymphohistiocytosis, Albinism (partial), recurrent pyogenic Infections by staphylococci and streptococci, peripheral Neuropathy. Giant granules in granulocytes and platelets. Pancytopenia. Mild coagulation defects.
53
Chronic granulomatous disease Defect presentation finding
Defect of NADPH oxidase. X linked susceptibility to catalase ⊕ organisms. ``` Abnormal dihydrorhodamine (flow cytometry) test (low green fluorescence). Nitroblue tetrazolium dye reduction test (obsolete) fails to turn blue. ```
54
Encapsulated bacteria
``` Encapsulated (Please SHINE my SKiS): Pseudomonas aeruginosa, Streptococcus pneumoniae, Haemophilus Influenzae type b, Neisseria meningitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, Group B Streptococcus. ```
55
Bacterias and micotic suceptibility when low granulocytes
Staphylococcus, Burkholderia cepacia, Pseudomonas aeruginosa, Serratia, Nocardia Candida (systemic), Aspergillus, Mucor
56
Virus that present with deficences of B cells
Enteroviral encephalitis, | poliovirus
57
Types of Transplant rejection
Hyperacute acute chronic Graft vs Host disease

USMLE 1 (73 decks)

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