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VET375 > Immunopathology > Flashcards

Immunopathology Flashcards

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1
Q

Where do immune cells originate from?
Name the 2 types

A

Hematopoietic stem cells (HSC)
- lymphoid progenitor cells
- myeloid progenitor cells

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2
Q

What do myeloid progenitor cells differentiate into?

A
  • megakaryocyte
  • eosinophil
  • basophil
  • neutrophil
  • monocyte (–> dendritic cells & macrophages)
  • mast cells
  • erythrocytes
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3
Q

What do lymphoid progenitor cells differentiate into?

A
  • T cells
  • B cells (–> plasma cells –> anitbodies)
  • NK cells
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4
Q

Name the main cell types of innate immunity

A
  • Phagocytes
  • NK cells and other ILCs
  • Complement proteins
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5
Q

Name the main cell types of adaptive immunity

A
  • B & T lymphocytes
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6
Q

Name the mechanisms of INNATE immunity that require activation before gaining effector functions

A
  • Phagocytosis
  • Degranulation
  • Amplification/Recruitment
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7
Q

Name the mechanisms of ADAPTIVE immunity that require activation before gaining effector functions

A
  • Antibodies (B and Th)
  • Cytotoxicity (Tc)
  • Amplification (cytokines)
  • Regulation (Treg)
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8
Q

How is the immune system initially activated? and what does it lead to?

A

PAMPS or DAMPS binding to PRRs
Leads to
- intracellular signaling - culminates in activation of transcription factors that move to the nucleus and up regulate the transcription of effector products of innate immunity (eg. cytokines and chemokines)
- phagocytic cells phagocytosing bacterial and killing them in phagolysomes

Pathogen associated molecular patters (PAMPs)
Damage associated molecular patterns (DAMPs)
Pattern recognition receptors (PRRs)

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9
Q

Where are PRRs located?

A
  • cell membrane - to detect intracellular pathogens
  • inside the cell - to detect intracellular pathogens
  • in circulation
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10
Q

Give 4 examples of inflammatory cytokines

A

TNF
IL1
IL6
IL 12

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11
Q

Give 2 examples of chemokines

A

IL 8
MCP-1

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12
Q

What links innate and adaptive immunity?

A

APCs (antigen presenting cells) and cytokines link innate and adaptive immunity

APCs - present antigen to lymphocytes to stimulate adaptive immunity
Cytokines - promote inflammation and contribute to activating lymphocytes

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13
Q

How are T and B cells activated? and what does it cause (3)?

A

APCs phagocytose a pathogen
Travel by lymphatics to the lymph node
APCs present antigens via the MHC complex to naive T cells in lymph nodes

Causes the following effector mechanisms:
- Activation of cytotoxic T cells (CD8+) = cytotoxic granule = DIRECT KILLING
- Activation and expansion of naive T cells = Effector T cells & Memory T cells
- Activation of B cells (via CD4+ T helper cells) = plasma cells = antibodies

*Examples of APCs: Dendritic cells, macrophage

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14
Q

What are the 2 types of CD4+ T helper cells?

A
  1. Th1 –> Cell mediated immunity & cytotoxicity (Induced by viruses or intracellular protozoa)
  2. Th2 –> Mediate humoral immunity esp synthesis of IgE (Induced by nematodes (and aeroallergens))

Produce different kind of cytokines and produce different immunological effects
Th1: IL-2, IFN-y
Th2: IL-4, IL-5, IL-9, IL-10, IL-13, IL-25, IL-31, IL-33

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15
Q

Explain the 4 types of effects cytokines can have

A
  • Endocrine - distant cell type
  • Paracrine - neighboring
  • Autocrine - binds to its own receptor
  • Juxtracrine - need to be in contact to work
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16
Q

What are cytokines?
What are the produced by?
Name 4 general properties

A

They are soluble mediators (chemical messengers) of the immune and inflammatory responses
Eg. Proteins, peptides, glycoproteins

Produced by nucleated (predominately immune) cells

  1. Pleiotropism - one cytokine - multiple functions
  2. Redundant - multiple cytokines - same function
  3. Synergistic - work together - sum is better than them done separately
  4. Antagonistic - opposite function - can turn things and off
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17
Q

4 types of cytokines and examples

A

PRO-INFLAMMATORY CYTOKINES
> IL 1
> type 1 interferons (Eg. IFN-a, IFN-b)
> IL 6
> TNF

CYTOKINES INVOLVED IN HAEMOATOPOIESIS AND LYMPHOCYTE DEVELOPMENT
> Numerous interleukins (IL-2, IL-3, IL-4, IL-5, IL-12, IL-15)
Some specific for Th1 bs Th2 response
> Transforming growth factor - b (TGF-b)
> Granulocyte macrophage colony simulating factor (GM-CSF)

CHEMOKINES
> IL-8
> Monocyte chemoattractant protein 1 (MCP-1)

ANTI-INFLAMMATORY CYTOKINES
> IL-10
> TGF-b

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18
Q

Define active and passive immunity and give examples of each

A

ACTIVE: Immunity that develops when the immune system actively responds to an antigen by producing its own antibodies and memory cells.
Eg. Vaccine or infection

PASSIVE: Immunity acquired by receiving pre-formed antibodies from another individual.
Eg. Via placenta or colostrum
Eg. Snake antivenom

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19
Q

Briefly describe the role of IgG immunoglobulins

Study These Flashcards
A
  • Major serum Ig
  • Diffuse readily into tissues
  • Largely unable to cross placental barrier in many species
20
Q

Briefly describe the role of IgM immunoglobulins

Study These Flashcards
A
  • First antibody formed as part of an immune response
  • 5 basic Ig units joined together!
  • Most remains within the bloodstream due to large size!
21
Q

Briefly describe the role of IgD immunoglobulins

Study These Flashcards
A
  • On the surface of immature B lymphocytes
22
Q

Briefly describe the role of IgE immunoglobulins

Study These Flashcards
A
  • Bound to surface receptors on mast cells and basophils
  • Antiparasitic activity
23
Q

Briefly describe the role of IgA immunoglobulins

Study These Flashcards
A
  • Important for mucosal immunity
  • Protected from enzymatic degradation by secretory piece
24
Q

Define immunopathology

Study These Flashcards
A

Refers to a defect or malfunction in either the innate or adaptive immune response that can result in disease and clinical illness

24
Name and briefly explain the 3 mechanisms of immunopathology
1. Immunodeficiency - ineffective immune response 2. Hypersensitivity - overactive immune response 3. Autoimmunity - inappropriate reaction to self
25
Name 3 general features of immunodeficiency
- ↑ susceptibility to infection - ↑ incidence of autoimmune disease - prone to virally-induced cancers
26
Name the 2 ways immunodeficiencies can be classified
1. by immune component --> Innate immune system deficiencies --> Adaptive immune system deficiencies 2. by cause/origin --> Primary - congenital inherited conditions --> Secondary - acquired
27
Name and briefly describe 2 primary/congenital INNATE immune system deficiencies
1. Chediak-Higashi syndrome - MECHANISM: mutation in the gene that regulates IC lysosomal trafficking - FUNCTIONAL DEFICIENCIES: abnormally large granules in granulocyte cells, enlarged pigment granules in melanocytes, impaired leucocytes function, also effects NK cells and platelets - CLINICAL ABNORMALITIES: recurrent infections, dilution of hair pigmentation, eye abnormalities (blindness), bleeding tendencies 2. Leucocyte adhesion deficiency - FUNCTIONAL DEFICIENCIES: neutrophils unable to migrate to extravascular sites, leukocytosis, recurrent bacterial infections
28
Name and briefly describe 1 primary/congenital ADAPTIVE B cell immunodeficiency
Agammaglobilinemia/hypogammaglobulinemia - MECHANISM: pre-B receptor checkpoint defect, defect in lymphocyte maturation - FUNCTIONAL DEFICIENCIES: ↓ serum Ig, ↓ B/absent cell numbers, no germinal centreslymphoid follicles in LNs, no plasma cells in tissues - CLINICAL ABNORMALITIES: recurrent infections, bacterial infections
28
Name 1 primary/congenital ADAPTIVE T cell immunodeficiency
DiGeorge syndrome (humans & mice)
29
Name and briefly describe 1 primary/congenital ADAPTIVE combined immunodeficiency
Severe combines immunodeficiency (SCID) - 100% fatal in Arabians! - MECHANISM: defect in enzymes involves in V(D)J recombination of T cell receptors (TCRs) and antibodies - STRUCTUAL & FUNCTIONAL DEFICIENCIES: hypoplasia of lymphoid organs, marked ↓ T cells in peripheral blood, normal or ↑ B cells, ↓ serum Igs - CLINICAL ABNORMALITIES: SCID in Arabian foals is 100% fatal from viral, bacterial or fungal infections
30
Name and briefly describe a cause of secondary/acquired immunodeficiency (the most common immunodeficiency in vet med)
Failure of passive transfer - affects ruminants, horses and pigs - causes >lack of colostrum ingestion by newborn >lack of colostrum production by dam >absorption failure by newborn - clinical signs >non specific eg lethargy >onser within few days of birth >fever >evidence of infection in specific locations eg. pneumonia, umbilical infection, joint infection - treatment - IV administration of plasma containing Igs (cannot give orally after 24hrs- bcs molecules are too big and wont be absorbed)
30
Name and briefly describe other causes of secondary/acquired immunodeficiency
- Medical interventioon eg chemotherapy - Infection of immune cells eg canine distemper virus, FIV, FeLV - Hypercortisolemia and stress eg intensive farming or hyperadrenocorticism - Chronic disease - due to lymphoid depletion - Environment - starvation/malnutrition - Old age - latrogenic immunosuppression eg administration of immune suppressant medication
30
Define immunological tolerance
Immunological tolerance is the state in which the immune system does not mount a response against specific antigens
31
What is autoimmunity?
An immune response directed against self-tissue, due to failure of self tolerance
32
Why does autoimmunity occur?
Dysregulation/imbalance of the immune system resulting in loss of self-tolerance is often multifactorial contributors include - Genetic predisposition - Other predisposing factors such as epigenetics (things that turn our DNA on and off) - Environmental triggers eg infection, exposure to drugs, vaccines etc
33
Explain the classification of immune mediated disease (IMD)
Primary - no obvious triggers - idiopathic Secondary - suspected secondary to a known trigger - sometimes removing the trigger resolves the disease - sometimes treatment is needed to 'reset' the immune system OR Non-associative - ie primary! Associative - is the issue incidental (just there at the same time?) - ie secondary - causative?
34
What is tolerance?
Failure of the immune system to respond to a pathogen
35
What is self-tolerance?
Failure of the immune system to respond to self-tissue antigens - A GOOD THING!
36
What are hypersensitivity reactions?
Undesirable/harmful responses produced by normal immune system mechanisms
37
Type 1 hypersensitivity reactions - Immunological component - Situations that trigger them - Mechanisms of injury - Pathological effects on tissues - Clinical consequences
- Immunological component: involves Th2 cells, IgE antibodies and mast cell - Situations that trigger them: Allergens - Mechanisms of injury: production of IgE antibodies - immediate release of vasoactive amines and other mediators from mast cells & recruitment of inflammatory cells - Pathological effects on tissues: vascular dilation, oedema, smooth muscle contraction, mucus production, inflammation - Clinical consequences
38
Explain the 2 stages of a type 1 hypersensitivity reaction
1. Sensitization - when individual is first exposed >Allergen exposure: A harmless antigen (e.g., pollen, food protein) enters the body. >Antigen presentation: Dendritic cells present the allergen to naive T helper cells, which differentiate into Th2 cells. >Th2 cell activation: Th2 cells release cytokines (e.g., IL-4, IL-13). >B cell activation: These cytokines stimulate B cells to class-switch and produce IgE antibodies specific to the allergen. >Mast cell sensitization: IgE antibodies bind to FcεRI receptors on the surface of mast cells and basophils, making them sensitized to the allergen. 2. Challenge - upon subsequent exposures to the same allergen and leads to clinical signs. > Allergen re-exposure: The allergen cross-links IgE molecules already bound to mast cells. >Mast cell degranulation: This triggers an immediate release of vaso reactive amines (eg. histamine) and also stimulates the arachidonic acid cascade and the production of lipid mediators >Degranulation and production of these products leads to the upregulation of inflammatory cytokines = BIPHASIC RESPONSE! 1st peak = preformed soluble mediators released from mast cells 2nd peak/later response = intracellular activation, up regulation of transcription then translation to produce proteins that get secreted as cytokines and chemokines
39
Type 2 hypersensitivity reactions - Immunological component - Situations that trigger them - Mechanisms of injury - Pathological effects on tissues - Clinical consequences
- Immunological component: IgG and IgM - Situations that trigger them: cell matrix associated antigens, cell surface receptors. Common causes: IMHA, transfusions, drug reactions, neonatal isoerythrolysis - Mechanisms of injury: production of IgG and IgM, bind to anitgen on target cell/tissue - causes damage in one of three ways 1. opsonization and phagocytosis of target cell 2. lysis of target cell by complement - membrane attack complex (MAC) 3. antibody dependent cell cytotoxicity - NK cell bind, releasing granules = apoptosis - Pathological effects on tissues: cell lysis, inflammation - Clinical consequences: depends on cell/tissue target > SELF - widespread tissue injury ie anemia, lethargy, fever, mucosal bleeding, ulceration, paralysis etc > FOREIN - hemolytic transfusion reaction|
40
Type 3 hypersensitivity reactions - Immunological component - Situations that trigger them - Mechanisms of injury - Pathological effects on tissues - Clinical consequences
- Immunological component: IgG and IgM - Situations that trigger them: soluble antigens ie bacterial or vial infection - Mechanisms of injury: deposition of antigen antibody complexes around the body = complement activation, recruitment of leucocytes by complement products and Fc receptors, release of enzymes and other toxic molecules - Pathological effects on tissues: necrotising vasculitis, inflammation - Clinical consequences: depends on site of immune complex deposition eg. glomeruli, blood vessels, synovial membrane of joint, uvea tract in the eye etc
41
Type 4 hypersensitivity reactions - Immunological component - Situations that trigger them - Mechanisms of injury - Pathological effects on tissues - Clinical consequences
- Immunological component: T lymphocyte mediated Situations that trigger them: Soluble antigen (eg bacterial or viral), contact antigens (eg poison ivy), cell-associated antigens - contact dermatitis, transplant rejection, tuberculosis, chronic allergic disease - Mechanisms of injury: activated T lymphocytes - release of cytokines and macrophage activation, T lymph mediated cytotoxicity - Pathological effects on tissues: perivascular cellular infiltration, oedema, cell destruction, granuloma formation - Clinical consequences: >PRIMARY/IDIOPATHIC: clinical manifestations of these condition are associated with organ specific derangement, more so than cell or tissue injury >SECONDARY: eg contact dermatitis - rash, pruritis etc - treatment involves removal of the trigger +/- immune suppression
42
What type of hypersensitivity is a bee sting?
Type 1
43
What type of hypersensitivity is IMHA?
Type 2

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