Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards Path > Immunology > Flashcards

Immunology Flashcards

1
Q

Lymph Node

A

Cortex is B cells. Primary follicle is dormant and secondary is active
-T cells in paracortex which communcates with HEV
-Plasma cells move to medulla to secrete Ab
-Medulla also location of dendritic cells and macrophages that can enter and exit the afferent and efferent vessels
-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

LN Drainage

A

Scrotum, anal canal below pectinate and thigh drain to superficial inguinal
-Testes and prostate to para-aortic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Spleen

A
  • Red pulp is fenestrated cappilaries to allow macrophages to remove damaged RBC from irculatin
  • White pulp has T cells in PALS and B cells in follicles interspersed
  • Autosplenectomy in sickle cell, also ruptured in mono and other trauma. Can be removed in spherocytosi
  • Increased risk of encapsulated bateria (SHINSKISS)
  • Strep Pneumo, H Flu, Nisseria, Salmonella, GBS, Klebsiella
  • If splenectomy there will be presence of howell jolley bodies that are RNA remnants, target cells
  • There will also be thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Thymus

A
  • Primary lymphoid organ derived from third pouch, DiGeorge 22q11
  • Cortex is double positive T cells from marrow that undergo positive selection to see if MHC works
  • Medulla contains dendrritic and epithelial cells (Hassalls Corpuscles) expressing AIRE that provide self antigens and generate self tolerance
  • Encapsulated organ in anterior mediastinum
  • Thymoma is Myasthenia Gravis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MHC I

A
  • Present on all nucleated cells, no RBC
  • Endogenous peptides placed in a groove, loaded in RER
  • A protein is TM and beta 2 microglobulin helps sustain structure
  • Interacts with CD8
  • Expression is increaed by IFN a and B
  • Main use against viral cells
  • A,B,C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MHC 2

A
  • Two transmembrane proteins A and B
  • Exogenous antigen loaded in endosome after CLIP invariant chain is lost in acid endosome
  • Expressed on antigen presenting cells
  • HLA DRQ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A3

A

Hemochormatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

B27

A

Males, MHC 1

-IBD, Ankylosing spondyltitis, Reiters, Psoriatic. RA negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DQ2 and DQ8

A

Celiacs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

DR2

A

Lupus, hay fever, MS, Goodpasteurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

DR3

A

DMI, Graves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

DR4

A

RA, DM1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DR5

A

Hashimotos, Pernicous Anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

NK Cells

A

CD16 (Fc receptor mediating ADCC) and CD 56 are markers
-Target cells with atypical or reeduced MHC I, kill by perforin and granzyme inducing apoptosis
-Highly active against tumor cells
-IL-2, 12, IFN a and b are major growth factors
-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

B Cells

A

Growth via IL-4 and 10

-Role in hyperacute, humoral acute, and chronic rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T Cells

A

-IL-2 is growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T Cell maturation

A

Precursors from bone marrow don’t contain TCR or MHC

  • Arrive in cortex with TCR (CD3) and CD8 and CD4
  • Positive selection in cortex to see if TCR interacts with MHC
  • Negative selection in cortex (Hassal’s corpuscles) to see if don’t recognize self proteins (AIRE)
  • CD8 will lead to CTL
  • CD4 can be stimulated by IL-12 to make TH1 and IL-4 to make TH2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Activation

A

Expression of MHC I on all nucleated cells and MHC 2 on

  • Dendritic cells (Only ones that can activate Naive T cells, live in skin and traffic and activate in LN)
  • B cells, Macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Naive T Cell Activation

A
  • Dendritic cells are necessary and activate CD4 and CD8 cells in the lymph nodes
  • Signal one comes from TCR and MHC interacting, second signal comes from B7 (dendritic cells) and CD 28 on T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

B Cell Activation

A

CD 4 cells will interact with MHC 2 presented on surface of B cells and induce activation and class swithcing

  • 2nd signal comes from CD40 on B cells and CD40L on T cells which allow for production.
  • If good then release IL-4 to cause Ig production
  • If bad then can use Fas BADD pathway to induce apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hyper IgM

A 
Defect in CD40/L that results in inability to class switch and affinity maturation leading to only IgM being produced. 
-Most commonly X linked in CD40L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TH1

A
  • Activated by IL-12 secreted from macrohpages
  • Secretes IFN gamma which activates Macrophages
  • Macrophages secrete IL-1, TNF alpha, and IL-12 to positive feedback on TH1 creating positive loop
  • IL-4 and IL-10 inhibit differentiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

TH2

A
  • Activated by IL-4
  • Secrete IL-4 (Ab and isotype switching)
  • IL-10: inhibit Th1
  • IL-5 Eospinophil tactic (ADCC)
  • IL-13: Class switching to IgE
  • Inhibited by IFNgamma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CTL

A

Express CD8 and interact with MHC 1 on all nucleated cells

  • If doesn’t recognize secrete porphorin and granzyme to acitvate Caspase 8 and apoptosis
  • Also contains FAS which induces apoptosis and controls immune response
  • Highly responsible for graft rejection and death of graft cells
  • Also can kill neoplastic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

T Regs

A

CD25 (IL-2 receptor)

  • FOXP3
  • Secrete IL-10 and TGF beta to tone down immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ab Structure

A
  • Light chain is kappa and lambda, rearranges second and is VJ recombination (occurs by RAGs)
  • Heavy Chain is VDJ rearrangment occurs with RAGs
  • TdT adds extra nucleotides when bring together to increase variability (not somatic hypermutation which occurs with AID)
  • Heavy chain contains complement and macrophage binding region
  • HC also contains FC receptor interaction region (Phagocytosis, ADCC)
  • Fab is antigen specificity and is light and heavy (idiotype)
  • Fc is isotype and only heavy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

IgG

A

Cross placenta, abundant in serum, phagocytose opsonize
-ADCC with NK cells only
IgG4 is a cause of systemic sclerosing llnesses like Riedel’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IgA

A

Secreted as a dimer at mucosal surfaces bound to PolyIg or secretory component that is picked up from epithelial cells during transcytosis

  • Can be present in serum as a monomer
  • Secreted in colostrum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

IgM

A

BCR

  • Secreted as a pentamer and is often low specificity
  • Best at activating complement, doesn’t cross placenta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

IgD

A

-On surface of B cells, often imature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

IgE

A
  • Secreted in resonse to IL-4
  • Physiologic role is ADCC from eosinophils, but can also play a role in type 1 hyperesnstivity
  • Binds to surface of basophils and mast cells and when crosslinked leads to release of hitamine and inflammatory markers
  • Basophils also play a role in parasitic infections and release IL-4 and histamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Thymus Independent

A
  • Non protein
  • LPS and capsular polysacharides
  • Can induce and immune response and secretion of IgM but can’t stimulate memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Thymus Dependent

A

-Protein antigens that can be expressed on MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Complement

A
  • 3 pathways all lead to production of
  • C3 convertase which produces C3a and C3b (B in opsin and 5 convertase and A is anaphylatoxin)
  • C5 convertase (C3b and others) leads to C5a and C5b
  • C5b complexes to create MAC and C5a is neutrophilotaxic and anaphylatoxin
  • Anaphylatoxins activate mast cells
  • C3b is necessary to clear immune complexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

PNH

A
  • Defect in GPI anchor that anchors DAF (Generally ccurs de novo mutation in HPSC in marrow), resides on X chromosome
  • Leads to decreased DAF which normally inhibits C3 convertase. This leads to MAC and lysis of RBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

C1 Esterase Deficency

A
  • Hereditery andiodema
  • INcreased activation of classical pathway leads to increase in C3a and C5a leading to swelling of face and eyes
  • Do not give ACE inhibitors as Bradykinin is activated by activated mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

C5-C9

A

Recurrent Nisseria Infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Early complement C1-C3 deficency

A
  • Leads to decrease C3 activation.
  • Decreaased C3b leads to impaired clearance of immune complexes and can predispose to lupus and type 3 hypersensitivity
  • Also higher risk for recurrent severe URI and sinus infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

IL-1

A
  • Secreted by Macs and T cells
  • Pyrogen and acute phase reactants
  • Increases expression of adhesion molecules (CAM on endothelium)
  • Also induces chemokine secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

IL-6

A

-Similiar to IL-1, pyrogen and acute phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

IL-8

A
  • Neutrophil tactic (Bacterial products, LTB4, C5a)

- Macrophage is the major source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

IL-12

A

Induce TH1 phenotype

Activates NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

TNF alpha

A
  • Main player in septic shock, causes endpthelilal activation, dilation, and leak
  • Acute phase and pyrogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

IL-2

A

Tophic for T cells, necessary for survival, drugs (SCID)

45
Q

IL-3

A

-Like GM-CSF, causes growth of HPSC

46
Q

IL-4

A
  • Causes TH2 differntiation

- B cells and class switching to IgG and IgE

47
Q

IL-5

A
  • Growth and chemotaxis of eosinophiles

- Also increases IgA prodcution

48
Q

IL-10

A

-Immunosuppressive especially on TH1

49
Q

TGF-B

A

Immunospressive, secreted by CD25 FOXp3 Postiiv cells

50
Q

IFN gamma

A
  • Induces antiviral state
  • Activats macrophages, NK cells, Neutrophils, TH1
  • Increases MHC expression
  • Can be used in CGD to increase intracelllar killing
51
Q

IFN a and B

A
  • Induce expression of ribonucleases that are specific for viral mRNA
  • Also decreases protein synthesis and divsion of cells
  • A is used in Hep C
  • B is used in MS
52
Q

Macrophage Surface Markers

A
  • CD14 is TLR4 that binds LPS and activates in the absence of other signals
  • MHC2 and CD7 (TH cells), CD40 (APC)
  • FcG receptor and C3b
53
Q

NK

A
  • CD16-ADCC

- CD56

54
Q

Superantigen Mechanism

A

-Crosslinks TCR and MHC2 leading to massive activation

55
Q

Endotoxin

A

-Binds CD14 and activates macrophages independent of cpstimulation. Leads to TNF alpha secretion and can cause DIC and shock in sepsis

56
Q

Ag variation

A

Salmonella: flagella
-Nisseria: Pillus
Borellia
Trypanasomes (Sleeping Sickness and Cruzi longterm infecions)

57
Q

Vaccine Differences

A

Live generates cell mediated and Killed generates humoral

58
Q

Type I Hypersensitivity

A
  • IgE binds to FcR on Mast (tissue) and Basophils (Circulating)
  • Leads to degranulation and release of vasoactive amines (Histamine, seretonin), IL-5, GMCSF, IL-3 etc
  • Also release lipid mediators
  • Hypotension shock
59
Q

Type 2 Hypersensitivity

A
  • Ab specific for target, generally cytotoxic but doesn’t have to be
  • Causes specific tissue mediated effects
  • Opsonization (Extravascular hemolysis)
  • Complement ativation (inflammatio)
  • ADCC (CD16 on NK cells)
60
Q

Type 3

A
  • Immune complexes are deposited in tissues when they fall out of blood
  • Activate complement leading to neutrophil chemotaxis and tissue injury
  • Lack of early complement components can predispose to lupus
61
Q

Arthus Reactions

A
  • Injection leads to very local accumulation of Ag leading to formation of local Ag Ab complexes that cause a very local edematous and necrotic lesion,
  • Commonly after recieveing a vaccine or passive immunization
62
Q

Serum Sickness

A
  • Systemic form of arthus, Drugs and Hep C can cause the precitpitation of Ab complexes throughout the body leading to vasculitis, arthtritis, proteinuira, lymphadenopathy
  • Drugs are the msot common cause
  • Takes days to develop (5)
63
Q

Type 4

A
  • Non humoral. T cells recognize Ag and activate macrophages that cause a local response
  • Contact dermatitis, PPD, MS, Transplants, Guillan Bare
  • IL-2 and IFNy are the main cytokine
64
Q

Blood Transfusions

A

Hyperkalemia from RBC lysis

  • Hypocalcemia from citrate
  • CMV is the most commonly transmitted infection, Hep C is also possible
65
Q

Anaphylaxis

A

-To IgA in patients who are IgA deficiecnt

66
Q

Nonhemolytic

A
  • Immune response to MHC antigens on leukocytes
  • Leads to fever, chills, etc, but there is no hemolysis
  • Type 2 hypersensitivity
67
Q

Hemolytic

A
  • ABO incompatability

- Leads to severe intra and extravascular hemolysis that is type 2 HS mediated

68
Q

Brutons Agammaglobulinemia

A
  • Defect in Tyrosine kinase present on X chromosome that is necessary for B cell maturation. Leads to no mature but normal immature B cells
  • No Ig will be made
  • Increaed Bacterial Infections after 6 months. Opsinization is crucial for clearance
  • Occurs from 6 months after birth (CVID can be acquired)
69
Q

B cell Deficencies

A
  • Have more bacterial infections than Viral/Fungal
  • Especially encapsulated
  • Increase risk of enteroviral infections (IgA) and giardiasis
70
Q

T cell Deficencies

A
  • Viral and Fungal infections, increase risk of sepsis

- Candida, PCP, Viral

71
Q

Granulocyte Deficencies

A
  • CGD: Aspergillus, Staph, Pseudomonas, Serretia, Nocardia

- If problem is in neutrophils can get candida dissemination

72
Q

Selective IgA

A
  • Unknown Cause, most common
  • Often assymptomatic but have increased mucosal infections, also have slight increase in autoimmune risk, also false positive B-HCG
  • Anaphylaxis with transfusion
  • Normal cell counts and other antibodies
73
Q

CVID

A
  • Inabiltiy to mature B cells, many causes
  • No mature B cells, no plasma cells, and no Ig
  • Chronic bacterial infections especially encapsulated
  • Commonly is acquired form muttion in HPSC
74
Q

THymic APlasia

A

Digeorge, absent thymic shadow and endodermal structues of 3rd and 4th pouch

  • Increased viral and Fungal (Candida and PCP)
  • Thymic independednt antigens can still cause response
75
Q

IL-12 receptor deficency

A
  • No TH1 cells leads to incresaed risk of viral, TB, inectonis
  • Disseminated TB is most common cause of death
  • There will be no IFN gamme because ther are no TH1 cells
76
Q

Hyper IgE (Jobs)

A

Defective TH1 secretion of IFN gamma leads to an increaese in TH2 response and an increase IgE

  • Hallmark is increased IgE leading to atopy and dermatitis.
  • Also will have impaired neutrophil cemotaxis and function leading to recurrent staph infections, failure to lose baby teeth
77
Q

Chronic Mucocutaneous Candidiasis

A
  • T Cell dysfunction

- ALso can be immunocupressants leading to dysfunction

78
Q

Defect in common gamma chain of IL receptors

A
  • Causes decrese in IL-2 R function leading to impaired immune in all fashions
  • X linked recessive
  • Absent thymic shadow and decresaed germinal centers
  • Decreased T circles (prodcut of recombination)
  • Recurrent infections with bacteria and virus, and fungal
  • Tx is BM transplant
79
Q

ADA deficency

A
  • Decreased recycling of Purines. No ADA leads to increased ATP this feedback inhibits ribonucleotide reductase leading to impaired GMP and pyrimidine synthesis
  • Same as SCID in gamma chain
80
Q

ATM

A
  • Defect in ATM gene that is required for DS break repaire
  • Cerebellar atrophy and ataxia, Spider angioma and telangectasia, IMmune deficecny, most commonly Ab deficency
  • AFP will often be elevated in early infant period
81
Q

Hyper IgM

A

Defect in CD 40 (B cells) or CD40L (T cells, more common, xlinked) leads to inability to class switch. Increase IgM and no other Ab present

  • Can’t affinity maturation
  • Most commonly bacterial infections
82
Q

Wiskott Aldrich Syndrome

A
  • Impaired actin reorganization leading to inabilty to signal through TCR
  • Thrombocytopenia, Eczema, Immunodeficency
  • Don’t give anticoagulants/aspirin
  • Patients also commonly have bloody diahrrea
83
Q

LAD

A
  • Defect in CD 18, integrin that is expressed on leukocytes
  • Leads to inability to bind tightly and inability to extravassae
  • Increase in number in the blood and decrease in tissues
  • Skin infections without pus
  • There is delayed separation of the umbilical cord
84
Q

Chediak Higashi

A
  • Defect in LYST an important protein for microtubule trafficking, can’t fiuse phagolysosomes
  • Leads to intracellular granules
  • Albino (Melanin granules), Neuropathy (NT vesicels), IMmunodeficecny
  • Especially staph and strep, can see large granules on EM
85
Q

CGD

A
  • NADPH oxidase turns oxygen into H2O2 that is then acted on by MPO to generate OCl in oxygen dependent killing
  • X linked
  • Can’t kill bugs that are catalase positive (Staph Aureus, Aspergillus, Psudomonas, Nocardia, Serretia)
  • NTB/Rhodamine will not turn blue
  • Can give IFN gamma to increase intracellular killing, also BM transplant is currative
  • If patient has same infections, but NTB test still works, the the patient may have MPO defcency
86
Q

Graft Rejection

A

-HLA molecules are codominantly expressed, so difficult to get right match, even in same family

87
Q

Hyperacute

A
  • Preformed Ab mediates Type 2 hypersensitivity and complement mediated RBC lysis
  • Vascular occlusion, ischemia, necrosis
88
Q

Acute

A
  • Days to weeks
  • CTL recognize MHC as foreign and begin killing, will see a dense lymphocytic infiltrate
  • Can be reversed with immunosupressants (Muromunab-3, Cyclosporin)
  • Vasculitis as generally starts in the edothelium
89
Q

Chronic

A
  • Months to years
  • Long term minimal killing of MHC percieved as foreign leads to endothelial injury, and progressive occluding fibrosis.
  • Humoral also plays a role
  • Inevitable in reality
  • Commonly seen in lungs as bronchiolitis obliterans (airway obstrucion leading to obstructive pattern, decreaed FEV1)
90
Q

GVHD

A
  • When implanted lymphocytes begin attacking host cells that are immunocompromised
  • Seen most commonly in bone marrow, but can also be seen in liver transplants
  • Generally starts with Jaundice, HSM and liver damage as well as maculopapular rash
  • May be beneicial in leukemia
91
Q

Cyclosporine

A
  • Binds Cyclophilins and inhibits caclinueirn induced NFAT activation of IL-2 and IL-2R leading to decrased T Cells Responses
  • S/E: Metabolic Syndrome, Gingival Hyperplasia, Hirsuitism, nephrotoxicity
92
Q

Tacrolimus

A
  • Binds FK proteins that leads to inhibition of Calcinueirn and decrased NFKB and IL-2 signalling
  • Metabolic sydrome and nephrotoxicity. No hirsuitism or gingival hyperplasia in contrast to Cyclosporine
93
Q

Sirolimus

A
  • Inhibits mTOR pathway that is the downstream signalling of IL-2 Receptor
  • S/E: Hyperlipidemia, thrombocytopenia, leukopenia
94
Q

Azathioprine

A
  • Antimeatbolite, active form is 6 mercaptopurine, inhibits purine synthesis and decreases B and T cell proliferation
  • Metabolized by xanthine oxidase, allourinol can make side effects worse
  • S/E: Bone Marrow Supression
95
Q

Muromunab-CD3

A
  • Binds CD3 TCR and prevents activation leading to lack of proliferation and death of T cells
  • Used in combo for organ transplants
  • S/E: cytokine release syndrome which is where cytokines are released and cause patient to feel sick.
96
Q

Aldesleukin

A
  • IL-2 analog

- Used to stimulate T Cells in cancer

97
Q

Filgrastim

A

-GCSF

98
Q

Saragrostim

A

-GMCSF

99
Q

Alpha interferon

A

-Hep B and C, Kaposi Sarcoma, Melanoma, leukemia

100
Q

IFN B

A

MS

101
Q

IFN Y

A

CGD

102
Q

Oprevlekin

A

IL-11 stimulates megakaryoytes

103
Q

Thrombopoetin

A

Stimulates megakaryoctyes

104
Q

Infliximab, Adalinumab

A

TNF alpha

105
Q

Abciximab

A

GP 2b3a

106
Q

Traztuzumab

A

Her2Neu

107
Q

Rituximab

A

CD20

108
Q

Altmetizumab

A

CLL

109
Q

Duclizumab

A

IL-2 Receptor

Boards Path (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions