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ACVECC Exam 2024 > Immunology > Flashcards

Immunology Flashcards

1
Q

Hospital acquired infection definition

A

Infection diagnosed >48 hours after hospital admission, more specifically on or after the third day in hospital without proven prior incubation

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2
Q

Independent risk factors for HAI

A

Prolonged length of hospital stay
Indwelling devices
Mechanical ventilation
Trauma
Individual patient factors/comorbidities

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3
Q

Two mechanisms by which bacteria are developing antibiotic resistance

A

Extended spectrum beta lactamases (ESBLs)
Plasmid-mediated AmpC enzymes

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4
Q

Factors associated with development of MDR E. coli

A

Hospitalization >6 days
Treatment with a cephalosporin prior to admission
Treatment with a cephalosporin <1 day
Treatment with metronidazole while in hospital

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5
Q

Factors associated with MDR E.coli and methicillin resistant Staph. aureus (MRSA)

A

Hospitalization > 3 days

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6
Q

Neutrophil behavior

A

Neuts move from circulation into the tissues by attaching first loosely then tightly to receptors in activated endothelial cells –> move between endothelial cells and pericytes into the interstitial space –> become activated when their pattern-recognition-receptors (PRRs) bind PAMPs on pathogens and DAMPs on dying cells –> once activated they begin degranulation

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7
Q

Three ways neutrophils kill

A
  1. Degranulate to release destructive peptides and proteases into the extracellular matrix or into an intracytoplasmic phagosome containing ingested bugs
  2. Assemble a reactive oxygen species generator (NAPDH oxidase complex) on the membrane of a phagosome or on the outer cell membrane which produces an oxidative burst when activated by microorganisms
  3. They form neutrophil extracellular traps (NETs) - DNA, histones, and other nuclear material combine with destructive peptides and proteases from intracytoplasmic granules and are expelled from the cell into the extracellular space; the NETs ensnare and kill pathogens and contain destructive molecules preventing damage to regional tissues. A process called “NETosis”.
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8
Q

Molecule that signals for neutrophil production

A

Cytokine granulocyte colony stimulating factor (G-CSF)

Most important cytokine for maintaining neutrophil homeostasis

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9
Q

What makes G-CSF

A

Bone marrow stromal cells
Also secreted by macrophages, monocytes, endothelial cells, fibroblasts

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10
Q

What drives “emergency myelopoiesis”?

A

Cytokine stimulation and the binding of PAMPs/DAMPs to PRRs on hematopoietic stem cells

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11
Q

What is a main factor for steady-state neutrophil production

A

The constant presence of PRR signaling in hematopoietic stem cells and progenitors stimulated by commensal microflora

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12
Q

Cytokines and growth factors that stimulate neutrophil release from the bone marrow

A

G-CSF
Granulocyte macrophage (GM)-CSF
TNF-alpha
TNF-beta
Complement 5a

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13
Q

Cytokines vs. Chemokines

A

Used for communication between cells vs. chemokine guide immune cells on where to go

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14
Q

Th1 cytokines

A

Type I immune response- drive by Type I T-helper cells- cellular immunity against intracellular pathogens- activation of CD8 T cells/NK cells/macrophages

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15
Q

Some of the cytokines involved in Th1/type I immune response

A

IL-2 (T cell survival, proliferation and differentiation)

IL-12 (activates NK cells)

TNF-alpha (can cause cell death)

LT-alpha (lymphotoxin-alpha)
LT-beta

IFN-gamma (antiviral, activates macrophages)

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16
Q

Th2

A

Type II immune response
Activates humoral responses (antibodies produced by B cells)

Strong presence of eosinophils, mast cells

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17
Q

Th2 cytokines

A

IL-4 (mast cell growth, stimulated eos)

IL-5

IL-13 (signals to make IgE)

IL-25

IL-10 (Ab production)

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18
Q

Three main lines of defense of the immune system

A

Physical barriers

Nonspecific (innate immunity)

Specific (adaptive immunity)

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19
Q

Where is the marginated pool of neutrophils

A

They roll slowly along the endothelium of smaller vessels and capillaries and tend to stagnate in post capillary venules; in dogs is about half of the total and in cats is 3/4 the total

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20
Q

Does the CBC measure the marginated or circulating pool

A

Circulating pool

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21
Q

Neutrophils have the (shortest/longest) half life in circulation

A

Shortest

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22
Q

Two bone marrow-centric mechanisms for neutropenia

A

Depletion of neutrophil progenitor cells (bone marrow hypoplasia)

Ineffective granulopoiesis (plenty of progenitors, they just aren’t working; maturational arrest, or retention/destruction of mature neutrophils in the bone marrow)

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23
Q

Infectious causes of depletion of granulocytic progenitor cells

A

Parvovirus
Ehrlichia canis (more often the cause compared to other rickettsial)
FeLV
FIV

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24
Q

FIV can also cause neutropenia because infected bone marrow cells secrete _____

A

Myelosuppression factors that depress granulopoiesis

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25
Q

Medications which can cause idiosyncratic neutropenia

A

Anticonvulsants
Methimazole
Colchicine

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26
Q

Main mechanism for neutropenia associated with myelophthisis

A

Decimation of bone marrow by infiltration of abnormal tissue –> loss of granulocytic progenitor cells

Loss of nurturing marrow microenvironment following destruction of bone marrow stromal cells

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27
Q

Cyclic hematopoiesis

A

“gray Collie syndrome”
Autosomal recessive
Severe neutropenia every 10-14 days
Mutation in the ELANE gene which encodes neutrophil elastase

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28
Q

Dysgranulopoiesis

A

Dysplastic granulocytes in the bone marrow in normal to excessive amounts, however peripheral neutropenia

Myelodysplastic syndrome (MDS)
Secondary dysmyelopoiesis
Congenital dymyelopoiesis

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29
Q

Myelodysplastic syndrome (MDS)

A

Mutated granulocytes do not follow normal maturation pathway and undergo apoptosis prior to release in circulation

Increased number of blasts in marrow

Can occur with FeLV

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30
Q

Secondary dysmyelopoiesis

A

Similar to MDS, but no increase in number of blasts in bone marrow

Can occur secondary to IMHA, ITP, lymphoma

Can also be seen following administration of certain drugs- chemo, phenobarbital, estrogen, cephalosporins, chloramphenicol, lithium in cats, colchicine

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31
Q

Trapped neutrophil syndrome in Border Collies

A

Hyperplastic granulopoiesis with no evidence of dysplasia/maturation arrest, but severe circulating neutropenia

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32
Q

Immune-mediated neutropenia

A

Antibodies are produced against neutrophil surface proteins and either activate complement-mediated death or opsonization and phagocytosis

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33
Q

Neutrophil count above which prophylactic antibiotics may not be necessary (unless febrile/sick)

A

0.75

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34
Q

How does G-CSF work

A

Increases differentiation of progenitor cells into neutrophils
Increases release of neutrophils into circulation
Acts on mature neutrophils to increase chemotaxis, enhance the respiratory burst, and improve IgA mediated phagocytosis

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35
Q

Initial PLT count is not correlated/predictive of survival; instead, presence of ____ at presentation is associated with poorer prognosis and higher requirement for transfusions

A

Melena

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36
Q

Proposed mechanism of ITP in dogs and cats

A

Increased phagocytosis by splenic macrophages due to autoantibodies bout to platelet integrin alpha-IIb-beta-3 (fibrinogen receptor) and glycoprotein Ib-IX (vWF receptor)

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37
Q

T/F: Thrombocytopenia severity in sepsis is associated with mortality

A

True

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38
Q

Two bacteria that can interact directly with platelets and cause platelet activation and aggregation

A

E. coli
Streptococcus

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39
Q

Canine platelet interactions with pathogens

A

Interact directly with pathogens by expressing functional TLR-4 which augments platelet activation in the presence of LPS and ADP

Once activated, platelets interact with circulating neutrophils to form NETs

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40
Q

Uremia-associated platelet dysfunction

A

Multifactorial
Due to defects in PLT adhesion, secretion, and aggregation
Diminished vWF binding activity (may look like type II vWF deficiency)

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41
Q

Platelet dysfunction/thrombocytopenia and liver disease

A

Decreased platelet aggregation in response to collagen and arachidonic acid - mechanism unknown

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42
Q

Broad drug categories that can affect platelet function

A

Anti-PLT drugs
NSAIDs
Drugs that increase cyclic nucleotides in PLT (pimo, sildenafil, theophylline/aminophylline)
Nitric oxide donors (nitroprusside, nitroglycerin)
Antithrombotics (heparin, factor Xa inhibitors)
Fibrinolytic drugs
Antimicrobials (beta lactams, cephalosporin)
SSRIs
Synthetic colloids
Vitamin E

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43
Q

Half-life of aspirin in dogs and cats

A

37.5 hours (cats)
8.5 hours (dogs)

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44
Q

Platelet inhibition with clopidogrel can last as many as _____ days

A

14 days

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45
Q

Rate-limiting enzyme in conversion of arachidonic acid to eicosanoids

A

Cyclooxygenase (COX)

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46
Q

PLT express mainly COX-1 or COX-2

A

COX-1

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47
Q

Expression of COX-2 by platelets is higher than normal during ______

A

Thrombopoiesis

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48
Q

Type I vWD

A

Deficiency of all vWF multimers
Dobermans

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49
Q

Type II vWD

A

Qualitative abnormalities in vWF

Four subtypes: 2A, 2B, 2M, 2N

Type 2A vWD (GSP’s) more severe bleeding diatheses

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50
Q

Type III vWD

A

Most severe form
Cats, some dog breeds (Chessies, Shelties, Scotties, Koikers)
Complete absence of vWF - spontaneous mucosal bleeding and life threatening bleeding after procedures/trauma

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51
Q

Glanzmann thrombasthenia

A

Mutation of ITGA2B gene which encodes the alpha-II-b subunit of the integrin alpha-II-b-beta-3
Without the receptor, fibrinogen binding and outside-in signaling do not happen –> severe hemorrhage following minor procedures

Otterhounds, Great Pyrenees

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52
Q

Bernard-Soulier syndrome

A

Glycoprotein Ib-IX-V complex abnormality

Macrothrombocytopenia and decreased PLT survival

Self-limiting mucocutaneous hemorrhage

Cocker Spaniels

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53
Q

Defective PLT agonist receptor

A

P2RY12 gene
Greater Swiss Mountain Dog

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54
Q

Chediak-Higashi

A

Autosomal recessive
Persian cats
Intrinsic platelet storage pool defect in the platelet dense granules, causing impaired PLT aggregation in response to collagen

Bleeding diatheses despite normal PLT concentration

Cats with oculocutaneous albinism

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55
Q

Alterations in PLT signal transduction pathways

A

Variants in CalDAG-GEF1 gene
Basset Hounds
Spits
Landseer

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56
Q

Canine Scott syndrome

A

German Shepherds
TMEM16F gene
Inability of phosphatidylserine to be externalized for creation of procoagulant membrane surface and facilitate thrombin generation

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57
Q

Definitive diagnosis of type I and II vWD

A

vWF antigen levels

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58
Q

Discontinuation of anti-platelet drugs prior to surgery - recommendations

A

D/c one (ideally clopidogrel) if on two, 5-7 days prior to procedure, in patients considered high risk for elective procedure

D/c anti platelet drugs 5-7 days prior if low risk bleeding

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59
Q

Tx for vWF deficiency

A

FFP: type I, II, or III

DDAVP: type I or II

Cryo: type I, II, or III

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60
Q

RBC changes associated with oxidative injury

A

Heinz bodies
Eccentrocytes
Pyknocytes

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61
Q

Pennies minted after ____ contain copper-plated ______

A

1982
Copper plated zinc

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62
Q

Osmotic fragility

A

Abysinninan and Somali cats
ESS

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63
Q

Phosphofructokinase deficiency

A

ESS
Cocker spaniels

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64
Q

Pyruvate kinase deficiency

A

Basenji
Dachshund
Mini poodle
Chihuahua
Pug
Westies
Labs
Somali cats
Abyssinian cats

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65
Q

Hemotropic mycoplasma in cats

A

Presumably transmitted via fleas
Cyclical, variable hemolysis
Can be Coombs positive

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66
Q

Babesia

A

Tick borne or blood borne

B. gibsoni (“small” babesia)
Pittbulls
Atovaquone azithromycin

B. canis (AKA vogeli) “large” babesia
Greyhounds
Imidocarb

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67
Q

Cytauxzooan

A

Tick

Hemolytic anemia
Fever
Organ failure from occlusion with schizont-laden monocytes
Atovaquone and azithromycin

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68
Q

Most common form of IMHA

A

Immunoglobulin mediated type II hypersensitivity reaction leading to extravascular hemolysis

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69
Q

Saline agglutination test

A

49 drops saline to 1 drop blood

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70
Q

Coombs test

A

Helpful when spherocytosis minimal and auto agglutination absent

Used to detect the presence of antibodies against circulating red blood cells (RBCs) in the body

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71
Q

Cat breeds in the US that are more likely to be type B blood

A

British Shorthair
Devon Rex
Abyssinian
Russian Blue
Somali

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72
Q

Classification of anaphylactic reactions

A

Immune-mediated (bites/stings, food, transfusion reactions)

Non-immune-mediated (heat/exercise)

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73
Q

Type I hypersensitivity

A

IgE
Mast cells
Soluble antigen
“anaphylactic”

Anaphylaxis, urticaria, hives, atopy, food allergy (peanuts in people)

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74
Q

Type II hypersensitivity

A

IgG
Cell or matrix-associated antigen
Phagocytes, NK cells
“cytotoxic”

IMHA, transfusion reactions

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75
Q

Type III hypersensitivity

A

IgG
“immune complex”
Soluble antigen
Phagocytes, complement

Serum sickness
Glomerulonephritis
Blue eye

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76
Q

Type IV hypersensitivity

A

T-cell mediated
Soluble, cell-associated antigen
Macrophages, eosinophils, cytotoxic T-cells

Contact dermatitis, flea and food allergy

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77
Q

Cell receptor on mast cells and basophils that the IgE antibodies bind to in type I hypersensitivity

A

Fc-episilon-R1

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78
Q

Non-immune-mediated anaphylaxis mechanisms

A

Does not require sensitization

Direct mechanical stimulation leading to mast cell degranulation

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79
Q

Mast cell degranulation products

A

Histamine
Tryptase
Heparin
Cytokines

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80
Q

Prostaglandins and anaphylaxis

A

Bronchoconstriction
Constriction of coronary and bronchial smooth muscle

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81
Q

Leukotrienes and anaphylaxis

A

Slower acting
Delayed response

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82
Q

Coagulation system and anaphylaxis

A

Release of platelet activating factor –> bronchoconstriction, increased vascular permeability, vasodilation, and platelet aggregation

Heparin from mast cells

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83
Q

Tryptase

A

Activates complement

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84
Q

Histamine receptors

A

H1: activates smooth muscle contraction and endothelial changes resulting in vasodilation and increased vascular permeability

H2: modulate gastric acid secretion and regulation of cardiac myocytes

H3: peripheral neurotransmitter release

H4: central neurotransmitter release

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85
Q

Cat lungs and anaphylaxis

A

Cat lungs have higher proportion of mast cells

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86
Q

Dog liver and anaphylaxis

A

Histamine alters blood flow
Concurrent arterial vasodilation and venous dilation

–> significant portal hypertension, transudation of fluid, and decreased venous return to the heart

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87
Q

Mechanism of shock in dogs with anaphylaxis

A

Mostly vasodilatory
Can also hypovolemic and cardiogenic

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88
Q

Epinephrine

A

a-1 receptor activity –> vasoconstriction (improved BP and coronary flow, improved upper airway obstruction and mucosal edema)

B-1 receptor activity –> inotropy, chronotropy, improved cardiac output

B-2 receptor activity –> bronchodilation and stabilization of mast cells (decreasing further degranulation)

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89
Q

Monocytes not only indicate inflammation, they also indicate ___ or ____

A

Tissue necrosis or an increased demand for phagocytes

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90
Q

A persistent eosinophilia and lymphocytosis occurs in __-__% of Addisonian patients

A

10-15%

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91
Q

Blood smear findings with liver disease

A

Non-regenerative anemia with acanthocytes
Target cells

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92
Q

Cellularity of normal CSF

A

<3 WBC/micro liter
NO neutrophils, plasma cells, macrophages

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93
Q

Mild to moderate predominantly mononuclear pleocytosis

A

Inflammatory diseases- often viral or rickettsial
Can also be seen with inflammatory brain disease, and IVDD

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94
Q

Moderate to marked predominantly neutrophilic pleocytosis

A

Infectious/inflammatory diseases such as bacterial ME, SRMA, FIP

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95
Q

Moderate to marked predominantly mononuclear pleocytosis

A

GME, breed-related necrotizing encephalitis (Pugs, Yorkers, Maltese, Chihuahuas)
Lymphoma

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96
Q

Marked pleocytosis with a predominance of eosinophils

A

Idiopathic eosinophilic meningitis
Parasitic migrations, protozoans, fungal disease

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97
Q

Mild to marked mixed pleocytosis

A

Fungal or protozoal ME
Infectious/inflammatory disease that is “aging” or being treated with medications that can alter cellular populations.
Necrosis due to infarction

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98
Q

Albuminocytological dissociation

A

When the total cell count is normal, but the protein level is high
Non specific

Degenerative or demyelinating diseases
Chronic IVDD/stenosis/neoplasia causing compression
Neoplasia

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99
Q

Normal stress leukogram findings

A

Neutrophilia
Monocytosis
Lymphopenia
Eosinopenia

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100
Q

Mechanism for neutrophila in stress leukogram

A

Shift from the marginating pool to circulating pool. A small amount may also be due to increased neutrophil release from BM and delayed apoptosis.
Since cats have a higher marginating pool, their neutrophilia can be more than 1:1 higher than the upper reference limit.

101
Q

Mechanism for Lymphopenia in stress leukogram

A

Decreased efflux from lymph nodes, decreased proliferation/active cytokines (such as IL-2) for lymphocyte and lymphotoxic effects (induction of apoptosis, usually this is chronic or with higher steroid doses)

102
Q

Eosinopenia, monocytosis mechanisms for stress leukogram

A

Monocytosis- unknown; maybe shift from marginating to circulating?

Eosinopenia- suspected to be decreased release from bone marrow

103
Q

Changes seen with physiologic leukocytosis (i.e. stress RESPONSE)

A

Most commonly seen in cats, and younger animals

Neutrophilia
Lymphocytosis
Eosinophilia, basophilia in cats

104
Q

Mechanisms for neutrophilia in physiologic leukocytosis

A

Shift from marginating to circulating

105
Q

Mechanism of lymphocytosis with physiologic leukocytosis

A

Release from the spleen

106
Q

Classic changes seen with inflammatory leukogram

A

Neutrophilia
Left shift
Toxic change
Monocytosis
Concurrent Lymphopenia (+/- eosinopenia)

107
Q

Thrombocytosis can be seen with inflammatory leukogram due to

A

Inflammatory cytokines such as IL-1 and IL-6

108
Q

Explain protein abnormalities that be seen in inflammatory states

A

Changes in albumin and globulins: This is usually comprised of low albumin or high globulin concentrations or a combination of both.

The low albumin concentration is due to a negative acute phase response (downregulation of production in hepatocytes) and the high globulin concentrations will be due to a positive acute phase response (increased production of α2 globulins by hepatocytes) or antigenic stimulation (polyclonal increase in immunoglobulins) or a combination of both.

109
Q

Hematocrit is calculated- what is the formula

A

HCT (%) = (MCV x RBC) /10

110
Q

Why is measurement of aggregate reticulocytes more reflective of regeneration in cats?

A

Aggregate retics last 12-24 hours vs. punctate last 7-21 days.

Punctate reticulocytes do not reflect the most recent bone marrow response (e.g. an anemic cat with only punctate reticulocytes is not actively regenerating at this time, but has shown some bone marrow regeneration in the past 7-21 days).

111
Q

Mechanism of anemia secondary to inflammatory disease

A

Cytokine suppression of erythropoiesis (decreased EPO release and response)

Hepcidin-mediated sequestration of iron

Decreased RBC lifespan (some component of hemolysis)

112
Q

NRIMA/PIMA bone marrow findings compared to PRCA bone marrow findings

A

PCRA- no or few erythroid precursors

PIMA- erythroid hyperplasia

113
Q

Fragmentation morphologies

A

Keratocytes, schistocytes, acanthocytes

114
Q

Proposed mechanisms for iron deficiency anemia (microcytic, hypo chromic; can be regenerative or non-regenerative)

A

1) Because immature RBC in the bone marrow stop dividing once a critical concentration of hemoglobin is reached within a RBC, deficient hemoglobin production will result in increased cell division. With each division, RBC become smaller, thus an iron deficiency anemia is characterized by microcytic and hypochromic RBC indices.
2) Iron deficiency affects enzyme activity which will alter receptor expression on erythrocytes which govern release. If iron deficient, the erythrocytes are no longer released and when they are retained in the marrow, they continue to divide. Later-stage RBC precursors do express Lutheran adhesion molecules, but there is no evidence to date that iron deficiency decreases their expression.
3) Possibly iron deficiency affects macrophages in marrow causing delayed extrusion of the nucleus of erythroid progenitors so they cannot be released from marrow (a protein in erythroblasts called erythroblast macrophage protein is required for extrusion and their interaction with macrophages).

115
Q

Cytokines that play a role in anemia of inflammation (anemia of chronic disease)- normocytic, normchromic

A

TNFα, IFNγ, IL-1β, and IL-6

116
Q

Anemia seen with chronic kidney disease mechanisms

A

Decreased EPO production
Increased hepcidin (–> iron sequestration)
Suppression of erythropoiesis (cytokines, uremia)
Decreased RBC lifespan (uremia)
Hemorrhage (uremia)
Malnutrition

117
Q

Pernicious anemia

A

Pernicious anemia is a relatively rare autoimmune disorder that causes diminishment in dietary vitamin B12 absorption, resulting in B12 deficiency and subsequent megaloblastic anemia. The anemia is megaloblastic and is caused by vitamin B12 deficiency secondary to intrinsic factor (IF) deficiency.

118
Q

Vitamin B12 functions

A

Within all eukaryotic cells, cobalamin acts as an essential cofactor for the intracellular enzymes methionine synthase and methylmalonyl-CoA mutase

119
Q

Pro-inflammatory cytokines

A

Released from Th-1 cells, CD4+ cells, macrophages, and dendritic cells

IL-1
IL-6
TNF-α

IL-2
IL-8
IL-12
IL-17
IL-18
IFN-γ

120
Q

Erythropoietin

A

Source: endothelium
Receptor: EpoR
Target cells: stem cells
Major function: RBC production

121
Q

G-CSF

A

Source: endothelium, fibroblasts
Receptor: CD114
Target cells: stem cells in bone marrow
Major function: granulocyte production
Classification: pro-inflammatory

122
Q

GM-CSF

A

Source: T cells, macrophages, fibroblasts
Receptor: CD116
Target cells: stem cells
Major function: growth/differentiation of monocytes, and eosinophil/granulocyte production
Classification: adaptive immunity

123
Q

IL-1

A

Source: macrophages, B cells
Receptor: CD121a
Target cells: B cells, NK cells, T-cells
Major function: pyrogenic, pro inflammatory, bone marrow cell proliferation
Classification: pro-inflammatory

124
Q

IL-2

A

Source: Th1 cells
Receptor: CD25
Target cells: Activated T and B cells, NK cells
Major function: proliferation of B cells, activated T cells; NK cell function
Classification: adaptive immunity

125
Q

IL-3

A

Source: T cells
Receptor: CD123, CDw131
Target cells: stem cells
Major function: Hematopoietic precursor proliferation and differentiation
Classification: adaptive immunity

126
Q

IL-4

A

Source: Th cells
Receptor: CD124
Target cells: B- and T-cells, macrophages
Major function: enhances MHC II expression, stimulates IgG and IgE production
Classification: adaptive immunity

127
Q

IL-5

A

Source: Th2 cells and mast cells
Receptor: CDW125, 131
Target cells: Eosinophils, B cells
Major function: B cell proliferation and maturation, stimulates IgA and IgM production
Classification: adaptive immunity

128
Q

IL-6

A

Source: Th cells, macrophages, fibroblasts
Receptor: CD126, 130
Target cells: B cells, plasma cells
Major function: B-cell differentiation
Classification: pro-inflammatory

129
Q

IL-7

A

Source: BM stromal cells, epithelial cells
Receptor: CD127
Target cells: stem cells
Major function: B and T cell growth factor
Classification: adaptive immunity

130
Q

IL-8

A

Source: macrophages
Receptor: IL-8R
Target cells: Neutrophils
Major function: chemotaxis for neutrophils and T cells
Classification: pro-inflammatory

131
Q

IL-9

A

Source: T cells
Receptor: IL-9R, CD132
Target cells: T cell
Major function: growth and proliferation
Classification: adaptive immunity

132
Q

IL-10

A

Source: T cells, B cells, macrophages
Receptor: CDw210
Target cells: B cells, macrophages
Major function: Inhibits cytokine production and mononuclear cell function
Classification: ANTI-inflammatory

133
Q

IL-11

A

Source: BM stromal cells
Receptor: IL-11Ra, CD130
Target cells: B cells
Major function: Induces acute phase proteins
Classification: pro-inflammatory

134
Q

IL-12

A

Source: T cells, macrophages, monocytes
Receptor: CD212
Target cells: NK cells, macrophages, tumor cells
Major function: Activates NK cells, phagocyte activation, endotoxic shock, cachexia, tumor toxicity
Classification: anti-inflammatory

135
Q

IFN-alpha

A

Source: macrophages, neutrophils
Receptor: CD118
Target cells: various
Major function: anti-viral
Classification: pro-inflammatory

136
Q

IFN-beta

A

Source: fibroblasts
Receptor: CD118
Target cells: various
Major function: anti-viral, anti proliferative
Classification: pro inflammatory

137
Q

IFN-gamma

A

Source: T cells and NK cells
Receptor: CDw119
Target cells: various
Major function: MHC-I and -II expression on cells, antiviral, macrophage and neutrophil function
Classification: pro-inflammatory

138
Q

TNF-alpha

A

Source: macrophages
Receptor: CD120a,b
Target cells: macrophages
Major function: phagocyte activation, toxic shock
Classification: pro inflammatory

139
Q

TNF-beta

A

Source: T cells
Receptor: CD120a,b
Target cells: Phagocytes, tumor cells
Major function: chemotactic, phagocytosis, oncostatic, induces other cytokines
Classification: pro-inflammatory

140
Q

TGF-β

A

Source: T and B cells
Receptor: TGF-βR1, 2, 3
Target cells: activated T and B cells
Major function: inhibits hematopoiesis, promotes wound healing, inhibits T and B cell proliferation
Classification: anti-inflammatory

141
Q

Anti-inflammatory cytokines

A

TGF-β
IL-10
IL-12
IL-22
IL-38 (IL-1F10)
IL-37 (1L-1F7)

142
Q

Bacterial lipopolysaccharides

A

LPS

PAMP found on cell membrane of gram-negative bacteria

Recognized by TLR 4

143
Q

Peptidoglycan

A

Another PAMP found on gram negative bacteria

Recognized by TLR2 (heterodimer of TLR1 or TLR6)

144
Q

Lipoteichoic acid (LTA)

A

Gram positive bacteria

Recognized by TLR2, and TLR1 or TLR6

145
Q

Bacterial lipoproteins (sBLP) from gram positive bacteria

A

Recognized by TLR2, and TLR1 or TLR6

146
Q

Phenol soluble factor from Staph. epidermidis

A

Recognized by TLR2, and TLR1 or TLR6

147
Q

Zymosan, a component within yeast walls

A

Recognized by TLR2, and TLR1 or TLR6

148
Q

DAMP- HMGB1

A

Cell nucleus
Receptor is TLR2, TLR4, RAGE

149
Q

DAMP- HMGN1

A

Cell nucleus
Receptor is TLR4

150
Q

DAMP- Defensins

A

Come from granules
Receptor is TLR4

151
Q

DAMP- Syndecans

A

Come from plasma membrane
Receptor is TLR4

152
Q

DAMP- Cathelicedin

A

Comes from granules
Receptor is P2X7, FPR2

153
Q

DAMP- heat shock proteins

A

Comes from cytosol
Receptors are TLR4, TLR2, CD91

154
Q

Alpha vs. beta defensins

A

a-defensins - produced constitutively
majority of b-defensins are inducible

a-defensins operate mainly from within phagosomes, whereas b-defensins are produced primarily by epithelial cells.

155
Q

Nuclear factor kappa beta

A

NF-kB signaling is one of the main down-stream path- ways responsible for HDP production.

NF-kB is a transcription factor involved in the integration of numerous parallel signaling pathways and a variety of cellular responses central to an immediate and functional immune response, including the production of cytokines and cell adhesion molecules

156
Q

LPS

A

Lipopolysaccharide fromthe Gram-negative bacterial cell wall has been demonstrated to induce inflammation by promoting pro-inflammatory cytokines and release of HMGB1 in innate immune cells

TLR4 is receptor

157
Q

LPS induced endotoxiemia in dogs

A

In dogs with experimentally induced endotoxemia, lipopolysaccharide (LPS)-treated dogs
had greater IL-6, IL-10, and tumor-necrosis factor-𝛼 (TNF-𝛼) concentrations during the first 24 hours after LPS administration compared
with dogs that received placebo

158
Q

Cell-free DNA

A

Cell-free DNA is a DAMP that
stimulates the immune system via TLR9

159
Q

Cytokines in dogs with sepsis (JVECC)

A

IL-6
CXCL8
KC-like
CCL2

All substantially increased compared to healthy controls

160
Q

GDV and HGMB1 levels

A

In dogs with GDV, high HMGB-1 concentrations were
associated with gastric necrosis and with nonsurvival

161
Q

CCL2

A

Chemokine (C-C motif) ligand 2 (CCL2) (also called monocyte chemoattractant protein-1) is a member of the C-C chemotactic cytokine family, and a potent chemotactic factor for macrophages

162
Q

Cytokines in sick cats (Frontiers 2020)

A

Revealed that sick cats (sepsis or septic
shock) had significantly higher plasma concentrations of IL-6, IL-8, KC-like, and RANTES
compared to healthy controls. The combination of MCP-1, Flt-3L, and IL-12 was
predictive of septic shock. None of the cytokines analyzed was predictive of outcome
in this study population.

163
Q

CRP, SIRS in dogs (JVECC 2018)

A

Conclusions – Serum CRP concentration is increased in dogs with SIRS, and decreases during treatment and hospitalization. Serum CRP, plasma IL-6, and plasma TNF-a =concentrations cannot predict outcome in dogs with SIRS.

164
Q

Use of pRBCs in dogs with IMHA (vs. whole blood)

A

Dogs with IMHA typically are euvolemic, making pRBC preferable to whole blood because the plasma provides no added benefit, increases the risk of volume overload, and may increase the risk of transfusion reaction.

165
Q

Downsides of bovine hemoglobin solutions

A

BHS scavenge nitric oxide, potentially activating platelets and causing vasoconstriction, which increases risk
of hypertension.3

BHS exert a greater colloid osmotic (oncotic)
pressure than do RBCs, increasing the risk of intravascular volume expansion and hypertension.

166
Q

Two statistically proven outcome factors on chemistry for dogs with IMHA

A

Bilirubin
BUN

167
Q

Rationale for anticoagulant drug administration in patients with IMHA

A

Thrombosis in IMHA predominantly affects the venous system, where thrombi form under low-shear conditions. Such thrombi typically are rich in fibrin, and their formation is less dependent upon platelet number or function, providing a rationale for administration of anticoagulant drugs.

168
Q

Poor prognostic factors in dogs with ITP

A

The presence of melena or high BUN concentration in the study suggested a poor prognosis for affected dogs.

169
Q

Platelet specific antibody

A

The PSAIgG assay is sensitive and specific for detecting platelet-bound antibodies; however, it does not discriminate between primary and secondary IMT, and positive results are possible in dogs with glomerulonephritis, neoplasia, hepatitis, or pancreatitis

170
Q

Immune dysfunction in critically ill dogs (JVIM 2028)

A

TLDR: These findings suggest dogs with CI develop immune system alterations that result in reduced respiratory burst function and cytokine production despite upregulation of TLR-4.

Immunologic evaluation: LPS-induced leukocyte production of TNF-a, IL-6, and IL-10 was significantly less in the CI group compared to the healthy dogs

Unstimulated (PBS) leukocyte production of TNF-a was reduced in the CI group compared to the healthy dogs

Compared to phagocytic cells from healthy dogs, phagocytic cells from the CI group had a significant decrease in oxidative burst function stimulated both biologically with E. coli and chemically with PMA

There was a significant increase in the percentage of monocytic cells expressing TLR-4 alone as well as co-expressing HLA-DR and TLR-4 in the CI group

One possible explanation for this observation includes the development of endo- toxin tolerance.

Upon binding of LPS, TLR-4 is activated to recruit the myeloid differentiation primary response protein 88 (MYD88) which subsequently induces the production of a variety of cytokines, including TNF-a, IL-6, and IL- 10, through various DNA transcription factors

171
Q

Skin physical barriers

A

Langerhans cells- macrophage system
Dry
Turn over rapidly
low pH
Calprotectin (metal chelator)
Pattern recognition receptors in keratinocytes = C type lectins, mannose receptors, TLRs
Microbiota

172
Q

Respiratory physical barriers

A

Mucus
SURFACTANT

Upper- IgE
Lower- IgG

Everywhere- IgA

173
Q

GI tract physical barriers

A

IgA
Mucus
Enterocytes, goblet cells (mucus), paneth cells
Peyer’s patches

174
Q

What in gram positive bacterial wall do PRRs recognize?

A

Peptidoglycans

175
Q

What in acid-fast bacterial wall do PRRs recognize?

A

Glycolipids

176
Q

What in yeast organism walls do PRRs recognize?

A

Mannan or beta-glucan rich cell wall

177
Q

What in viruses do PRRs recognize?

A

Nucleic acids

dsRNA= TLR-3
ssRNA= TLR-7, TLR-8
dsDNA= TLR-9

178
Q

On what cells are TLRs found

A

Sentinel cells of innate immune system (macrophages, neutrophils, mast cells, dendritic cells)
T and B cells of adaptive immune system
Non-immune cells (epithelial cells that line the respiratory and GI tract)

When they’re turned on –> INFLAMMATION

179
Q

Location of TLR receptor and its purpose/what it recognizes

A

Outer surface - bacteria

Inside cell in endoscopes - viruses, bacterial nucleic acids

180
Q

Gram positive bacteria PAMPs

A

Peptidoglycans
Lipotechoic acid
Lipoprotein

181
Q

Acid fast bacteria PAMPs

A

Glycolipids
Mycolic acid
Galactic

182
Q

Yeasts PAMPs

A

Mannan or beta gluten rich cell wall

183
Q

Viruses PAMPS

A

Nucleic acids
dsRNA - TLR3
ssRNA - TLR7, TLR8
dsDNA - TLR9

184
Q

How does a TLR get activated

A

PAMP binds TLR
TLR activates MyD88
NF-kappa beta activates genes –> IL1, IL6, TNF alpha –> inflammation
IRF3 activates genes –> type I interferons –> virus inhibition

185
Q

TLRs located on outer surface of cells (recognize bacteria)

A

TLR1/2 (recognize triacetylated lipoproteins)
TLR2/6 (recognize diacetylated lipoproteins)
TLR4 (recognizes LPS)
TLR5 (recognizes flagellin)
Dectin-1 (recognizes B-glucans)
RAGE (recognizes HMGB1)

186
Q

TLRs located in endosomes within cells (recognize viruses, bacterial DNA)

A

TLR3 (recognizes dsRNA)
TLR7 and TLR8 (recognize ssRNA)
TLR9 (recognizes CpG DNA)

187
Q

TLR1

A

Located on cell surface
Recognizes triacetylated lipoprotein on BACTERIA

188
Q

TLR2

A

On cell surface
Recognizes lipoproteins on bacteria, viruses, parasites

189
Q

TLR3

A

Located inside the cell in endosomes
Recognizes dsRNA of viruses

190
Q

TLR4

A

Located on cell surface
Recognizes LPS (bacteria, viruses)

191
Q

TLR5

A

Located on cell surface
Recognizes FLAGELLIN on bacteria

192
Q

TLR6

A

Located on cell surface
Recognizes diacetylated lipoproteins on bacteria, viruses

193
Q

TLR7

A

Located inside the cell
Recognizes ssRNA and guanosine on viruses (and some bacteria)

194
Q

TLR8

A

Located inside the cell
Recognizes ssRNA of viruses and some bacteria

195
Q

TLR9

A

Located inside cell
Recognizes dsDNA, CpG DNA (viruses, bacteria, protozoa)

196
Q

TLR10

A

Located inside the cell; regulates TLR2 responses
SUPPRESSES INFLAMMATION

197
Q

TLR11

A

Located on surface of cell
Recognizes profilin, flagellin on protozoa and bacteria

198
Q

TLR12

A

Located on cell surface
Recognizes profilin of protozoa

199
Q

What are nod-like receptors (NLRs)

A

PRRs
Nucleotide binding oligomerization doman receptors

Detect INTRACELLULAR PAMPs

200
Q

What does NOD1 recognize

A

Bacterial peptidoglycans

201
Q

What does NOD2 recognize

A

Bacterial muramyl dipeptide
General sensor of intracellular bacteria

202
Q

Downstream action of NLR activation

A

NF-kB –> pro inflammatory cytokines
NOD2 –> defensins (antimicrobial proteins)

203
Q

What are dectins

A

PRRs
Cell surface glucans
Bind to fungi

204
Q

Bacterial peptidoglycans are recognized by

A

TLRs, NODs, CD14

205
Q

Types of sentinel cells

A

Macrophages, dendritic cells, mast cells

Specifically: Kuppfer cells in the liver, splenic macrophages, microglial cells of CNS, alveolar macrophages (dust cells), langerhans cells of skin

206
Q

TNF-a produced by sentinel cells in response to TLR stimulation results in

A

Inflammation (induces IL1, 6 and 8 production)
Causes signs of inflammation
Later, facilitates transition from innate to adaptive immunity

207
Q

Production of interleukin-1 is secondary to stimulation of ___ and ___

A

CD14 and TLR4

208
Q

Production of IL6 from macrophages is in response to ___, ___ and ___

A

IL1
Endotoxins
TNF-a

209
Q

Actions of IL6

A

Promotes inflammation
Increases hepcidin formation (anemia of chronic inflammation)

210
Q

Histamine

A

Major source: mast cells, basophils, platelets
Function: increases vascular permeability, pain

211
Q

Serotonin

A

Produced in platelets, mast cells, basophils
Function: increased vascular permeability

212
Q

Kinins

A

Major source: plasma kininogens and tissues
Function: vasodilation, increased vascular permeability, pain

213
Q

Prostaglandins

A

Major source: arachidonic acid
Function: vasodilation, increased vascular permeability

214
Q

Thromboxanes

A

Major source: arachidonic acid
Function: platelet aggregations

215
Q

Leukotriene B4

A

Major source: arachidonic acid
Function: neutrophil chemotaxis, increased vascular permeability

216
Q

Leukotriene C, D, E

A

Major source: arachidonic acid
Function: smooth muscle contraction, increased vascular permeability

217
Q

Platelet activating factor (PAF)

A

Major source: phagocytic cells
Function: platelet secretion, neutrophil secretion, increased vascular permeability

218
Q

FDPs

A

Major source: clotted blood
Function: smooth muscle contraction, neutrophil chemotaxis, increased vascular permeability

219
Q

C3a and C5a

A

Major source: serum complement
Function: meat cell degranulation, smooth muscle contraction, neutrophil chemotaxis (C5a)

220
Q

What are 3 ways that antibodies participate in host defense?

A

Neutralization - IgA - bind pathogens and render them innate; important for viral protection (not aggressive enough for bacteria)

Opsonization - IgG, IgE, C3b, C5b - coat pathogens with Ab to facilitate phagocyte ingestion

Complement activation

221
Q

Complement proteins and their main sources

A

Hepatic - C3, C6, C8
Macrophages - C2, C4, C5
Mast cells - C1q
Neutrophil granules - C6, C7

222
Q

Three complement pathways

A

Antigen-antibody reaction - “classical” - Ab+C1q

Mannose binding protein- “lectin” pathway- MBL+MASP-2

Bacterial endotoxin- “alternative” pathway

223
Q

All three pathways lead to activation of ____ which ultimately results in downstream activation/production of membrane attack complex

A

C3

224
Q

Examples of organisms that activate the “alternate” pathway of complement activation (mannose binding lectin pathway)

A

Salmonella
Candida
Neisseria

225
Q

Function of C3b and C4b

A

Opsonization –> activate neuts/macrophages –> phagocytosis

226
Q

Actions of C5B6789 (membrane attack complex)

A

Ruptures bacterial cell wall, leading to lysis

227
Q

Complement that leads to chemotaxis (3)

A

C3a –> attracts eosinophils
C5a –> attracts neutrophils and macrophages where antigen is present
C567 –> attracts neutrophils and eosinophils

228
Q

Complement that leads to blood coagulation

A

C5a –> enhances coagulation, inhibits fibrinolysis; induces expression of tissue factor and plasminogen activator inhibitor I
Thrombin acts on C5a to generate C5a

229
Q

Complement (3) that activate mast cells

A

C3a, C4a, C5a –> release of inflammatory mediators (histamine, serotonin)

230
Q

Canine C3 deficiency (Brittany Spaniels)

A

Hereozygotes- normal
Homozygotes- no detectable C3
–> Lower IgG levels
–> Infection (Clostridium, Pseudomonas, E. coli, Klebsiella)
–> Immune complex mediated kidney disease**
–> Amyloidosis

231
Q

Lifespan of a neutrophil

A

Short
7-10 hours

232
Q

Neutrophil emigration

A

Endothelial cells express P-selectin
L-selectin on neutrophils binds P-seslctin
Chemokinds and leukotrienes trigger neutrophils to express leukocyte function-associated antigen 1 (LFA-1)
LFA-1 binds intercellular adhesion molecule-1 (ICAM-1) on endothelial cells
Bind PECAM-1 and then diapedese into tissues

233
Q

How long to monocytes circulate in blood before migrating to the tissues where they become macrophages?

A

~3 days

234
Q

Which chemokine does macrophages make that attracts neutrophils

A

CXCL8 (IL8)

235
Q

Macrophages are activated by ___, ___, and ___

A

IFN-y
TNF-a
IL2

236
Q

What triggers fever

A

IL1, IL6, TNF-a

237
Q

Thermostatic set point alteration

A

COX-2 in the hypothalamus –> PGE2 production –> new set point

238
Q

IL1 and IL6 trigger production of hepcidin in the liver, which then binds _____ in enterocytes to prevent iron absorption

A

Hepcidin

239
Q

____ is a protein that tags circulating iron (hemoglobin) for macrophage destruction

A

Haptoglobin

240
Q

Macrophages in the liver/spleen make _______ which helps steal bacterial siderophores preventing their uptake of iron

A

Lipocalin-2 (Siderocalin) AKA NGAL

241
Q

All leukocytes have cell marker (CD) _____

A

CD45

242
Q

Which cluster of differentiation (CD) marker is on B-lymphocytes

A

CD19

243
Q

All T lymphocytes have CD ___

A

CD3

244
Q

Cytotoxic T cells have _____

A

CD8- receptor for MHC I

245
Q

Helper T cells have ____

A

CD4 - receptor for MHC II

246
Q

Activated T lymphocytes have CD ____

A

CD25

247
Q

Primary immune response antibody vs. secondary immune response antibody

A

IgM is high primary (such as with first vaccine)
IgG is high secondary (booster)

248
Q
A

ACVECC Exam 2024 (26 decks)

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