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Immunology Flashcards

1
Q

primary immune system organs

A

Bone Marrow - B cell maturation

Thymus - T cell differentiation and maturation

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2
Q

secondary immune system organs

A

Spleen, lymph nodes, tonsils, peyer patches allow immune cells to interact with antigens

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3
Q

Lymph node

A

nonspecific filtration by macrophages
Storage of B and T cells
Immune response activation

Follicle - B cells

Paracortex- T cells. Endothelial venules which allow T and B cells to enter from blood. Enlarges in extreme immune response

Medulla - medullary cords (lymphocytes and plasma cells) and medullary sinus (reticular cells and macrophages, also communicates with efferent lymphatics)

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4
Q

Spleen

A

Red pulp - sinusoids which are long vascular channels

White pulp - T cells in Periarteriolar lymphatic sheath (PALS). B cells are found in follicles (White pulp -> white blood cells)

Marginal zone - between red and white pulp contains macrophages and specialized B cells. This is where antigen presenting cells (APCs) capture blood borne antigens for recognition by lymphocytes

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5
Q

Splenic dysfunction/postsplenectomy findings

A

decrease IgM –> decrease complement activation –> decrease C3b opsonization –> increase susceptibility to encapsulated organisms

Postsplenectomy: Howell -jolly bodies, target cells, thrombocytosis, lymphocytosis

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6
Q

opsonization

A

Antibody opsonization is the process by which the pathogen is marked for ingestion and eliminated by the phagocytes.

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7
Q

Thymus

A

THymus = THird pharyngeal pouch

Cortex - immature T cells

Medulla- mature T cells and hassal corpuscles containing epithelial reticular cells

Normal neonatal thymus is “sail shaped” on CXR

Thymoma - myasthenia gravis and superior vena cava syndrome

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8
Q

Innate immunity

A

neutrophils, macrophages, monocytes, dentritic cells, natural killer cells, complement, physical epithelial barriers, secreted enzymes

Resistance does not change throughout organisms lifetime

nonspecific, rapid, no memory response

secretes lysozymes, complement, c reactive protein (CRP), defensins

Pathogen recognition via toll like receptors (TLRs) - recognize pathogen associated molecular patterns (PAMPs) and lead to activation of NK-kB (i.e. LPS in gram -)

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9
Q

Adaptive immunity

A

T cells, B cells, Circulating antibodies

Variations through the V(D)J recombination during lymphocytes development

Resistance is not heritable, highly specific, refined over time, memory response

Secretes immunoglobulins

Memory cells: activated B and T cells

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10
Q

Major histocompatibility complex I

A

1 loci: encoded by the HLA-A,B, and C genes

Binds T cell receptors (TCRs) and CD8 on CD8+ cytotoxic T cells

1 long chain and 1 short chain ( 3 alpha, 1 Beta)

Antigen loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing)

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11
Q

Major histocompatibility complex II

A

2 loci: encoded by HLA-DP, DQ, and DR

Binds TCRs and CD4 on CD4+ helper T cells

Antigen laoded following release of invariant chain in an acidified endosome

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12
Q

MHC I diseases

A

HLA-A3 : Hemochromatosis
HLA-B8 : addison disease, myasthenia gravis, graves disease (dont be l8te dr. addison, or youll send my patient to the grave)
HLA-B27: Psoriatic arthritis, Ankylosing spondylitis, IBD-associated arthritis, Reactive arthritis

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13
Q

MHC II diseases

A

HLA-DQ2/DQ8: Celiac disease (cant eat DQ ice cream)
HLA-DR2: multiple sclerosis, hay fever, SLE, goodpasture (2-3 SLE)
HLA-DR3- DM type I, SLE, Graves disease, hashimoto , addison disease (2-3 SLE)
HLA-DR4: Rheumatoid arthritis, diabetes mellitus type 1, Addisons disease “ 4 walls in the rheum”
HLA-DR5: hashimoto thyroiditis (Hashimoto is an odd doctor DR3 and DR5)

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14
Q

Natural killer cells

A

perforin and granzymes induce apoptosis

Also by anibody dependent cell mediated cytotoxicity (CD16 binds Fc region of bound Ig activating the NK cells)

enhanced by IL2, IL12, IFN alpha, IFN beta

induce to kill when exposed to nonspecific activaion signal or absence of MHC I

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15
Q

B cells

A

humoral immunity
recognize antigen, produce antibody by differentiating into plasma cells to secrete specific immunoglobulins, maintain immunological memory

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16
Q

T cells

A

Cell mediated immunity

CD4+ t cells help B cells
CD8+ T cells directly kill

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17
Q

Differentiaton of T cells

A

1) T cell precursor in the bone marrow
2) in the cortex of the thymus we have positive selection where T cells expressing TCR capable of binding self-MHC on coritcal epithelial cells survive
3) In the medulla of the thymus we have negative selection where T cells with TCRS that have high affinity for self antigens undergo apoptosis or become regulatory T cells
4) move to lymph nodes where CD8+ T cells become cytotoxic T cells and CD4+ T cells become Helper T cells
5) Helpter T cells –> Th1, Th2, Th17, Treg

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18
Q

TH1

A

+ IL 12 and IFN gamma
- IL 4 and IL 10

secretes IFN gamma

Activates macrophages and cytotoxic T cells to kill phagocytosed microbes

THis is enhanced by the T cell CD40L interacting with CD 40 on macrophages

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19
Q

TH2

A

+ IL 2 and IL 4
- IFN gamma

Secretes IL-4, IL-5, IL-6, IL 10 , IL 13

activates eosinophils and promotes production of IgE for parasite defense

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20
Q

TH17

A

+ TGF beta and IL-6
- IFN gamma and IL 1 and IL6

secrete sIL 17, IL 21 IL 22

immunity against extracellular micorbes through induction of neutrophilic inflammation

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21
Q

Treg

A

+ TGF beta
- IL-6

Secretes TGF beta and IL 10 and IL 35

Regulatory T cells that produce anti antiinflammatory cytokines

prevents autoimmunity by maintaining tolerance to self antigens

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22
Q

Regulatory T cells

A

are identified by expression of CD3, CD4, and CD25, and FOXP3

IPEX syndrome ( Immune dyregulation, polyedocrinopathy, enteropathy, X linked) - geneticdeficiency in FOXP3

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23
Q

T cell activation

A

Dendritic cell migrates to the lymph nodes to present the antigen

T cell activation (signal 1) : antigen is presented on the MHC and recognized by the TCR of the Th Cell.

Proliferation and survival (signal 2) : B7 protein (CD80/86) on the dendritic cell and the CD28 on the naive T cell interact

Th cell activates and produces cytokines

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24
Q

B cell activation

A

After the Th cell activates

B cell is an antigen presenting cell

Foreign antigen is present on the MHC II and recognized by the TCR on the Th cell

CD40 receptor on the B cell binds CD40 ligand on the Th cell

Th cell secretes cytokines that determine Ig class switching of B cell –> B cell begins antibody production

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25
Antibody structure
Fab consists of light and heavy chains and recognizes antigens Fc region of igM and IgG fixes complement. All heavy chain
26
Fab region of antibody
Fragment, antigen binding Variable and hypervariable regions Unique antigen binding pocket
27
Fc region of antibody
constant region, carboxy terminal, complement binding, carb side chains, determines iso type (igM, IgD)
28
Mature naive B cells prior to activation express?
IgM and IgD they eventually isotype switche in lymph nodes into plasma cells that secrete IgA, IgE, or IgG
29
IgG
secondary response to an antigen Fixes complement Opsonizes bacteria neutralizes toxins and viruses ONLY isotype that crosses the placenta and provides infants with passive immunity
30
IgA
``` prevents attachment to mucous membranes does not fix complement Monomer in circulation Dimer with J chain when secreted Gi tract, tears, saliva, mucus, and breast milk ```
31
IgM
Primary response to an antigen (immediate) | Fixes complement
32
IgE
binds mast cells and basophils Immediate (type I) hypersensitivity immunity to parasites b activating eosinophils
33
thymus independent vs thymus dependent antigens
independent lacks a peptide component | dependent contains a protein component
34
Complement
plays a role in innate immunity and inflammation
35
C3b C3a,C4a,C5a C5a
C3b binds bacteria (opsonization) C3a,C4a,C5a - anaphylaxis C5a-neutrophil chemotaxis
36
MAC?
membrane attack complex defends against gram _ bacteria Cytolysis C5b-9
37
Opsonins
C3b and IgG are the two primary ones in bacterial defense
38
Inhibitors
decay accelerating factor (DAF aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells
39
Paroxysmal nocturnal hemoglobinuria
defect in PIGA gene prevents formation of anchors for complement inhibitors such as DAF/CD55 and membrane inhibitor of reactive lysis )MIRL/CD59) Causes complement mediated lysis of RBCs
40
IL 1
"Hot T-Bone stEAK" for 1,2,3,4,5,6 IL 1 is HOT for fever Secreted by macrophages
41
IL 2
"Hot T-Bone stEAK" for 1,2,3,4,5,6 IL 2 is for T cells stimulation Secreted by T cell
42
IL3
"Hot T-Bone stEAK" for 1,2,3,4,5,6 IL3 is for bone marrow stimulation Secreted by T cell
43
IL4
"Hot T-Bone stEAK" for 1,2,3,4,5,6 IL4 is for IgE secreted by Th2 cells to induce differenciation of T cells into Th2 cells Promotes growth of B cells and enhances class switching to IgE and IgG
44
IL5
"Hot T-Bone stEAK" for 1,2,3,4,5,6 IL4 is for IgA production Growth and stimulation of eosinophils
45
IL6
"Hot T-Bone stEAK" for 1,2,3,4,5,6 aKute phase protein production secreted by macrophages
46
IL8
neutrophils secreted by macrophages
47
IL 12
T cells into Th1 cells activates NK cells secreted by macrophages
48
TNF alpha
causes WBC recruitment and vascular leak. activates the endothelium granulomas in TB mediates fever and sepsis along with IL1 and IL6
49
IL 10
decreases expression of MHC class II and Th1 cytokines TGF beta and IL10 both attenuate the immune response
50
Respiratory burst
rapid release of reactive oxygen species from different types of cells activation of phagocyte NADPH oxidase complex which utilizes O2 as a substrate NADPH plays a key role in both CREATION and NEUTRALIZATION Of ROS
51
Respiratory burst rxn
Inside phagolysosome O2 + NADPH --- NADPH oxidase --> O2*- O2*- is super oxide anion --superoxide dismutase ---> H2O2 H2O2 + Cl- ---Myeloperoxidase--> HClO* NOTE: myeloperoxidase contains a blue-green heme containing pigment that gives sputum its color HClO* is hydroxyl- halide radicals which degrades bacteria
52
Patient with whose phagocytes cannot kill some types of bacteria and fungi due to a deficieny of what enzyme in the oxidative burst/respiratory burst?
NADPH oxidase phagocytes of patients with chronic granulomatous disease can utilize H2O2 generated by invading organisms and convert it to ROS Increased risk of infection by catalase + species because they neutralize their own H2O2 leaving phagocytes without ROS for fighting infections
53
Interferons
INTERFERE with RNA and DNA viruses synthesized by cirus infected cells that act on local cells to prime them for viral defense how? - downregulating protein synthesis to resist potential viral replciation - upregulating MHC expression
54
T cell surface proteins
TCR CD3 CD28 binds B7 on APC
55
Helper T cells surface protiens
CD4 CD40L CXCR4/CCR5 (coreceptor for HIV)
56
cytotoxic surface proteins
CD8
57
Regulatory T cells surface proteins
CD4 | CD25
58
B cell surface proteins
``` Ig CD19 CD20 CD21 (receptor for EBV - "bar" drinking age is 21) CD40 MHC II B7 ```
59
MAcrophage surface proteins
``` CD14 (receptor for PAMPS like LPS) CD40 CCR5 MHC II B7 (CD80/86) Fc and C3b receptors (enhance phagocytosis) ```
60
NK cell surface proteins
CD16 | CD56 (marker for NK)
61
Hematopoietic stem cells
CD34
62
Anergy
state where a cell cannot become activated by exposure to its antigen (i.e. no costimulatory signal) example of self tolerance
63
Passive immunity
By receiving preformed antibodies from someone else to protect from infection (i.e. IgA in breast milk, materla IgG, antitoxin etc) Rapid and short lived protection Give preformed antibodies to pt afer exposure to tetanus toxin, botulinum toxin, HBV, Varicella, Rabies virus, or diphtheria toxin
64
Active immunity
Exposure to foreign antigens (i.e. natural infection, vaccines etc.) Slow but long lasting protection/memory
65
Live attenuated vaccine
No pathogenicity but retains ability for growth Induces cellular and humoral responses Given for "Attention! Please Vaccinate Small Beautiful Young Infants with MMR Regularly" 1) adenovirus 2) Polio virus 3) Varicella 4) Smallpox 5) BCG 6) Yellow Fever 7) Influenza 8) MMR 9) Rotavirus
66
Killed or inactivated vaccine
Pathogen is inactivated but maintains epitope structure on surface antigen Induces humoral response Safer but weaker and rewures booster shots RIP Always = Rabies, Influenza, Polio, Hep A
67
Subunit
Includes only the antigens that best stimulate the immune system HBV via HBsAg HPV (types 6,11,16,18) etc.
68
Toxoid
Denatured bacterial toxin with intact receptor binding site protects against bacterial toxins without risk of disease i.e. clostridium tetani
69
Type I hypersensitivity
ABCD 1234 Type 1 --> A --> Anaphylactic and Atopic Two phases: 1) Immediate (minutes) - antigen crosslinks preformed IgE on presensitized mast cells 2) Late (hours): chemokines (attract inflammatory cells/WBCs) and cytokines cause inflammation and tissue damage Example: allergen specific IgE test
70
Type II hypersensitivity
ABCD 1234 Type 2 --> AntiBody mediated Antibodies bind to cell surface antigens causing cellular destruction (cell is opsonized and then either phagocytosis, complement activation, or Nk cell killing occurs), inflammation due to complement system activation and Fc receptor mediated inflammation, Cellular dysfunction due to abnormal blockade of activation of downstream process Direct coombs test - detects Ab DIRECTLY attached to RBC surface Indirect coombs test- detects Ab unbound in the serum
71
Type III hypersensitivity
ABCD 1234 3--> immune Complex antigen antibody (mostly IgG) complexes activate complement complement attracts neutrophils which release lysosomal enzymes Examples: SLE, polyarteritis nodosa (systemic necrotizing inflammation of small and medium BV), poststrococcal glomerulonephritis Serum sickness- antibodies to foreign proteins Arthus reaction - local subacute immune complex mediated hypersensitivity reaction after intradermal injection of antigen into presensitized individual
72
Type IV hypersensitivity
ABCD 1234 4--> Delayed (also technically last one) Two mechanisms involving T cells ( DOES NOT INVOLVE ANTIBODIES): 1) direct cell cytotoxicity: CD8+ cytotoxic T cells kill targeted cells 2) inflammatory reaction: effector CD4+ T cells recognize antigen and release inflammation inducing cytokines 4 Ts: T cells,Transplant rejection, TB skin test, Touching (contact dermatitis)
73
Blood transfusion rxn: allergic/anaphylactic rxn
Type I hypersensitivity If IgA deficient then must receive blood products without IgA
74
Blood transfusion rxn: Febrile nonhemolytic transfusion reaction
1) Due to type II hypersensitivity rxn to donor HLA and WBCs OR 2) Due to Cytokines that are created and accumulate during the storage of blood products
75
Blood transfusion rxn: Acute hemolytic transfusion rxn
Type II hypersensitivity rxn intravascular hemolysis due to ABO blood group incompatibility Extravascular hemolysis due to foreign antigen on donor RBCs
76
Blood transfusion rxn: Transfusion related acute lung injury
Donor anti-leukocyte antibodies against recipient neutrophils and pulmonary endothelial cells
77
Autoantibody: Myasthenia gravis
Anti-Ach receptor
78
Autoantibody: Lambert Eaton Myasthenic syndrome
Anti-presynaptic voltage gated calcium channel
79
Autoantibody: SLE
ANA (non specific) Anti-cardiolipin Anti-dsDNA Anti-smith
80
Autoantibody: Rheumatoid arthritis
``` Rheumatoid factor (Igma against IgG Fc region) Anti-CCP (more specific) ```
81
Autoantibody: Sjogren syndrome
(Body's immune system attacks its own healthy cells that produce saliva and tears) Anti-Ro/SSA Anti-La/SSB
82
Autoantibody: Scleroderma (diffuse)
Anti-Scl-70 (anti DNA topoisomerase I)
83
Autoantibody: Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (churg strauss syndorome), uncerative colitis
MPO-ANCA/ PANCA
84
Autoantibody: granulomatosis with polyangitis (Wegener)
PR3-ANCA/CANCA
85
Autoantibody: Hashimoto thyroiditis
Antimicrosomal antithyroglobulin antithyroid peroxidase
86
Autoantibody: Graves disease
Anti-TSH receptor
87
Autoantibody: Celiac disease
IgA anti-endomysial IgA anti-tissue transglutaminase IgA and IgG deamidated gliadin peptide
88
Autoantibody: Type 1 diabetes mellitus
Anti glutamic acid decarboxylase | Islet cell cytoplasmic antibodies
89
Autoantibody: Pernicious anemia
Antiparietal cell, anti-intrinsic factor
90
Autoantibody: Goodpasture syndrome
Anti-glomerular basement membrane
91
Pt is a 8 month old baby boy that present with recurrent bacterial and enteroviral infections. He has no B cells and no Lymph nodes. He was healthy for the first 6 months
X linked (Bruton) agammaglobulinemia --> Boys Defect in BTK gene (tyrosine kinase) No B cell maturation Live vaccines contraindicated
92
Pt presents with Giardiasis and low IgA but normal IgG and IgM levels
Selective IgA deficiency ``` Asymptomatic Airway and GI infections Autoimmune Atopy Anaphylaxis to IgA ```
93
Pt is a 2 year old and presents with low plasma cells and low immunoglobulins
Common Variable immunodeficiency Defect in B cell differentiation
94
Pt presents with tetany and recurrent infections. His labs show low T cells, low PTH, and low Calcium. Also has conotruncal abnormalities.
Thymic aplasia (DiGeorge syndrome) 22q11 deletion Failure to develop 3rd and 4th pharyngeal pouches resulting in absent thymus and parathyroids
95
Pt received the BCG vaccine and now has disseminated mycobacterial and fungal infections. He is also noted to have low IFNγ levels
IL-12 receptor deficiency which decreases the Th1 response IFNγ - functions as the primary activator of macrophages, in addition to stimulating natural killer cells and neutrophils.
96
Upon examination it is noted that the patient has a cold/noninflamed staphylococcal abscess and retained primary teeth. He also has dermatologic problems like eczema. His labs show increased IgE and eosinophils.
Job syndrome - Autosomal Dominant hyper-IgE syndrome STAT3 mutation Deficiency of Th17 cells and thus impaired recruitment of neturophils to sites of infections
97
Pt presents with noninvasive candida albicans infections of skin and mucous membranes. However, he has no T cell proliferation or cutaneous reaction to it.
Chronic mucocutaneous candidiasis T cell dysfunction - defects in IL17 and IL17 receptor
98
Pt presents with failure to thrive, chronic diarrhea, and thrush. Also has recurrent viral, bacterial, fungal, and protozoal infections. On CXR he lacks a thymic shadow. On lymph node biopsy he lacks germ cells. On flow cytometry there are no T cells
Severe Combined Immunodeficiency (SCID) Defective IL-2R gamma chain OR adenosine deaminase deficiency Bone marrow transplant curative because no concern for rejection.
99
Pt presents with cerebellar defects (Ataxia). On physical exam its noted that he has spider angiomas/telangiectasia. His labs show low IgA levels
Ataxia-telangiectasia Defect in the ATM gene --> failure to detect DNA damage and halt profession of cell cycle. Mutations accumulate Pt presents with the triad (AAA) of Ataxia, spider Angiomas, IgA Labs show high AFP but low IgA IgG and IgE
100
Pt presents with severe pyogenic infections early in life. Also noted to have opportunistic infections with pneumocystitis, cryptosporidium, CMV. Labs show high IgM but very low IgG, IgA, IgE
Hyper IgM syndrome Defective CD40L on Th cells --> class switching defect Failure to make germinal centers
101
Pt presents with thrombocytopenia, eczema, and recurrent (pyogenic) infections
Wiskott-aldrich syndrome ``` Think WATER - Wiskott-Aldrich syndrome Thrombocytopenia Eczema Recurrent infections ``` low to normal IgG or IgM but high IgE and IgA
102
Pt is a newborn that presents with recurrent skin and mucosal bacterial infections. Pus is absent. It has been over 30 days and his umbilical cord has not yet seperated
Leukocyte adhesion deficiency (type 1) Defect in LFA-1 integrin (CD 18) protein on phagocytes Increased neutrophils in blood but absent in infection sites
103
pt is partialy albino and presents with progressive neurodegeneration, lymphohistiocytosis, recurrent infections by staph and strep, peripheral neuropathy.
Chediak Higashi syndrome Defect in lysosomal trafficking regulator gene (LYST) microtubule dysfunction in phagosome lysosome fusion Giant granules in granulocytes and plateletes. Pancytopenia
104
pt that is increasingly susceptible to catalase + organisms and has a positive dihydrohodamine (flow cytometry) test (decreased green fluorescence)
Chronic granulomatous disease Defect of NADPH oxidase that decreases reactive oxygen species and thus decreases respiratory burst in neutrophils
105
Immunodeficiency in B cells tends to produce recurrent ?
bacterial infections especially encapsulated ones (Please SHINE my SKiS) ``` Pseudomonas aeruginosa Streptococcus pneumo Haemophilus Influenza type b Neisseria meningitidis Escheridchia coli Salmonella Klebsiella pneumoniae Group B strep ```
106
Immunodeficiency in T cells tends to produce more?
fungal and viral infections
107
``` Grafts- Autograft Syngeneic graft (isograft) Allograft Xenograft ```
autograft is from self syngeneic graft (isograft) is from twin or clone Allograft is from same species Xenograft is from different species
108
Hyperacute transplant rejection
within minutes Type II hypersensitivity pre-exiting recipient antibodies react to donor antigen MUST remove graft
109
Acute transplant rejection
Weeks to months cellular response: Type IV hypersensitivity reaction. CD4+ and CD8+ T cells activate against donor MHCs Humoral: antibodies that develop after transplant prevent/reverse with immunosuppressants
110
Chronic transplant rejection
Months to years Type II and type IV hypersensitivity reactions CD4+ T cells respond to recipient APC presenting donor peptides (including MHC) Dominated by arteriosclerosis
111
Graft vs host disease
Varying onset Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with "foreign bodies" --> severe organ dysfunction Type IV hypersensitivity reaction pt presents with maculopapular rash, jaundice, diarrhea, hepatosplenomegaly

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