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Bloc F - Defense > Immunology > Flashcards

Immunology Flashcards

1
Q

What is an antigen?

A

something that induces and immune response (protein)

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2
Q

What is an Epitope?

A

the smallest component of an antigen that is recognized by the immune system (you react to that, not the drug itself)

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3
Q

What is an Antibody?

A

aka immunoglobulin-serum protein is produced by B cells –> plasma cells that bind antigen

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4
Q

What are Cytokines?

A

Proteins released by cells that modulate the behavior of other cells.

EX:
- Interleukins are one family of cytokines and are released by cells that attract other cells to the area

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5
Q

What are the functions of the immune system?

A
  1. fight infections
  2. prevent cancer
  3. develop a memory response
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6
Q

What are the 2 “types” of immune systems?

A
  1. Innate (0-4 days, NK, PMN, macrophages, eosinophil)
  2. Adaptative (acquired, T cells, B cells and antigens)
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7
Q

What happens after a barrier injury?

A
  1. Innate immune system kicks in (fast and first)
  2. Dendritic cells takes samples all over the body and takes it back to the CD4+ T cell so that is can recognize when an immune reaction needs to happen and WHICH reaction needs to happen (viral, bacterial…).
  3. The acquired immune system reacts to the specific attack
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8
Q

Lines of defense of the body?

A
  1. The first line of innate defense of the immune system is the skin, hair/cilia, saliva/tears, mucous, stomach acids and bile
  2. The second line of innate defense are initiated when host cells are damaged or when microbial structures are recognized: INFLAMMATION induced by mediators (prostaglandins, leukotrienes and bradykinins) Þ vasodilate, increase vascular permeability and recruit cells to the area of damage
  3. The innate immune mediated protection players come into action: neutrophils, macrophages, dendritic cells, eosinophils, basophils, mast cells and NK cells
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9
Q

Communication mechanisms of the immune system?

A
  1. Disruption of barrier that induces inflammation
  2. Pattern recognition receptors (PRRS): innate cells recognize common microbial footprints and rapidly respond to the perceived danger
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10
Q

Important cytokines?

A
  • IL-1: acute-phase protein secretion
  • IL-2: Important for growth
  • IL-6: acute-phase protein secretion
  • CXCL-8 (IL-8): Diverts immune response to TH1, pro-inflammation and cytokine secretion
  • TNF-alpha: Changes in vascular endothelium
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11
Q

What is the complement system?

A

The complement system is a series of proteins, found in plasma, that are involved in recognition of surface structures on pathogens, inflammation, activation of innate cells and killing and clearance of pathogens and products of inflammation from the body, thus preventing damage

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12
Q

Pathways of the complement system?

A
  1. Classical: antigen
  2. Alternative: pathogen surface
  3. Lectin: recognizes the lectin at the surface of pathogen
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13
Q

What happens when a naive T cell recognizes a peptide?

A

Its surface changes:

  • cytokine receptors eg IL2R
  • adhesion molecules eg CD28
  • chemokine receptors eg CCR3,4,5

And then it multiplies by the help of cytokines

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14
Q

Major Histocompatibility Complex (MHC) class I function?

A
  • Presents as an antigen when infected
  • Degrade viral invaders and other pathogens in a proteasome
  • Recognized by CD8+ T-cells
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15
Q

MHC Class II role?

A
  • Expressed by professional APCs (monocytes/macrophages, B cells, dendritic cells, Langerhans cells, Kupfer cells, and astrocytes)
  • Can pick up antigens, process them and present to CD4+ T cells
  • They are exported in acidic environment in endosomic vesicle
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16
Q

Dendritic cells’ role?

A

Have a large number of innate immune receptors –> engulf and process Ag, and process them for T cell by digestion into peptides to take it to the T cells

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17
Q

Comment les T cells peuvent-elles se rafiner?

A

By exposure to pathogens

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18
Q

What elements must T cells have in order to recognize an antigen?

A
  1. A receptor that can recognize a specific peptide (TCR)
  2. A signaling complex (CD3)
  3. A CD4 or 8 molecule
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19
Q

What are the roles of T cells?

A
  1. Fight intracellular infections: CD8 cytotoxic T-cells Þ directly fight viral and fungal infections different by inducing apoptosis (cytotoxicity)
  2. Assist other cells by activating them and helping them multiple or differentiate: CD4+ effector T-cells Þ Th1 (intracellular organisms), Th2 (parasite, allergy), Th9, Th17 (antibacterial, antifungal) ARE HELPERS
  3. Provide signals that inhibit or slow down inflammatory responses: Regulatory T-cells from both pathways (CD8 and CD4+)
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20
Q

IgM antibody?

A
  • 10% of circulating Ig’s
  • 1st antibody made (“defaut setting for B cells”)
  • Excellent at complement fixation
  • Good at neutralization
  • cytokine and environment dependent
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21
Q

IgG antibody?

A
  • 75% of all circulating antibodies
  • Main Ig produced in secondary antibody responses
  • Only antibody that crosses the placenta
  • Most pass actively in 3rd trimester
  • Good at fixing complement (IgG3 > IgG1 > IgG2 >> IgG4
  • Excellent opsonization (Fcg receptors)
  • Some IgG at mucosal surfaces
22
Q

IgA antibody?

A
  • 15-20% of circulating Ig
  • Lines mucosal surface : excellent 1st line of defense
  • Most common immune deficiency (1:700)
23
Q

IgE antibody?

A
  • Very low amounts in serum
  • Most IgE is bound to mast cells + basophils (FceR)
  • Key Ig in parasite defence
  • Responsible for allergy and anaphylaxis
24
Q

IgD antibody?

A
  • Little circulating
  • No clear role in host defense
  • Important marker of B cell maturation
25
Q

What do B cells require to elicit a strong antibody response?

A
  • Antigen
  • T cells for direct contact (usually TH2 cells)
  • Soluble cytokines (eg) IL4 + IL13, INF-g or IL10)
  • Certain adhesion molecules esp CD40
26
Q

Role of antibodies in defence?

A
  • Opsonization
  • Complement Activation
  • Neutralization
  • Antibody Dependent Cellular Cytotoxicity:
27
Q

What are b cells and their role?

A
  • A type of lymphocyte
  • Recognize foreign substances (antigens) via B-cell receptors (BCR) on their surface that look like antibody molecules (surface Ig or sIg)
  • Present Antigens to T-cells and secrete Antibodies!!
  • Produce Cytokines
  • B cells home to areas of antigen dependent maturation (e.g.) lymph nodes, spleen, to interact with T cells and specialized Follicular Dendritic Cells
  • Antibodies of increased affinity for better immune responses are produced through mutation of their BCR genetic program (somatic mutation) Þ only high affinity ones survive
28
Q

HOW does B cells recognize antigens?

A
  • B cells recognize three dimensional structures of antigens –> one antigen, many potential antibodies BUT for one B-cell = one antibody
  • Because they are antigen presenting cells, they internalize antigens and process them into peptides
  • T-cells are presented these peptides via MHC II to the TCR and then the T-cells send other signals to the B-cell that produces antibodies
29
Q

How does B cells develop?

A
  • Come from bone marrow
  • In a primary follicle, there is naïve B-cells who have not seen antigen. B cells mature into one of two pathways:
  1. Memory B cells: responds rapidly to antigens matures rapidly, and stored in secondary follicles
  2. Memory plasma cells: most mature subtype of B cell-produces and stores copious amounts of Ig and cytokines
30
Q

What are the primary (central) lymphoid organs?

A
  1. Bone marrow
  2. Thymus
31
Q

What does a bone marrow contain?

A

pluripotential hematopoietic stem cells (CD34+) –> progenitor hematopoietic cells and precursors of blasts –< B-lymphoblats –> B-CELLS that will mature in peripheral lymph node

32
Q

How are T cells produced in the thymus?

A
  1. T-lymphoblast from bone marrow – Cortex –> T-lymphoblasts –> T CELLS (CD4 and CD8) + macrophages –> positive selection
  2. Medulla Þ MATURE T CELLS (CD4+, CD8+ and CD20+) –> negative selection
33
Q

Structure of a lymph node?

A
  1. Sub-capsule: first place of metastasis, naïve cells
  2. Cortex: B-cells, follicles/germinal centers
  3. Paracortex: T-cells, NO follicles/germinal centers, high endothelial venules (HEVs)
  4. Medulla: memory B- and T-lymphocytes, plasma cells
34
Q

What is the journey of lymph?

A

Afferent lymphatic –> subcapsular sinus –> cortical sinuses –> medullary sinuses –> efferent lymphatic

**Parallel to steps in germinal center (GC) reaction to Ag

35
Q

What are the secondary (or peripheral) lymphoid organs?

A
  • Lymph nodes
  • Spleen
  • Mucosa-associated lymphoid tissue (MALT), including Waldeyer ring (tonsils, adenoids…), Peyer patches in ileum…
    Functions: defense of internal passages against foreign invaders, 70% of body’s immune cells
36
Q

What are the B-cell immune responses?

A
  1. Early primary immune response: Occurs outside the germinal center, in paracortex
    T-cell-independent activation of naïve B-cells to proliferating B-immunoblasts –> short-lived IgM-secreting plasma cells, but no memory cells
  2. Secondary immune response: occurs mostly inside the germinal center (GC)

Later (3-7 days), T-cell-dependent activation of naïve B-cells to proliferating B-centroblasts –> centrocytes –> immunoblasts –> IgG-secreting

37
Q

What are the plasma cells responses?

A
  1. IgM-secreting plasma cells short lived (1o response)
  2. IgA, IgG-secreting plasma cells long lived (2o response)
38
Q

What are the T cells immune responses?

A

Occurs in paracortex of lymph nodes, periarteriolar sheath of spleen, extranodal sites

  1. Ag presented to T-cells by APCs
  2. CD4 or CD8 on T-cells bind to MHC class II or class I, respectively, on APCs
  3. Mature T-cell –> T-immunoblast –> Effector CD4+ helper cells + Effector CD8+ cytotoxic cells + Memory T-cells
39
Q

What are the 4 key steps in germinal center (GC) reaction to Ag?

A
  1. Proliferation: inactivate BCL2 anti-apoptotic gene Þ apoptosis facilitated
  2. Somatic hypermutation of Ig V region genes Þ increase affinity of Ab for Ag
  3. Selection
  • Centroblasts mature Þ centrocytes Þ light zone GC
  • Ig heavy chain class switch: IgM Þ IgG or IgA
  1. Differentiation: into memory cells+ plasma cells
40
Q

Causes of fever?

A
  1. Infections
  2. Rheumatic diseases – autoimmune,
  3. Tissue damage eg trauma, MI
  4. Malignancies
  5. Endocrine – thyrotoxicosis
  6. Immune reactions eg transfusion reactions, drug reactions
  7. Autoinflammatory diseases
41
Q

Advantages of fever?

A
  • Some bacteria grow more slowly at a temperature of 40
  • Increased temperature decreases the availability of iron, required by bacteria for growth.
  • Increased temperature may inhibit replication of some viruses
  • The bactericidal ability of PMN’s is increased at elevated temperature
  • Activated dendritic cells move more quickly to the regional lymph nodes due to activation of adhesion factors
  • “Sickness behavior” limits spread of infection
42
Q

Inconvenients of fever?

A
  • CO2 production
  • Water loss
  • Cerebral injury
  • Discomfort
  • Seizure activity?
  • Each degree C of temperature increase increases O2 requirement 11-13 %
  • Where there is brain injury, fever can exacerbate the injury
  • Fever phobia
43
Q

Pathogenesis of fever?

A
  • Release of cytokines such as IL-1β, IL-6, TNF-α, and interferons acting as endogenous pyrogens
  • The initial response thought to be mediated by ceramide release in neurons in the anterior hypothalamus
  • The late response is mediated by coordinate induction of COX-2 and microsomal PGE synthase-1 in the endothelium of blood vessels in the preoptic hypothalamic area to form PGE2GE2
  • PGE2 can cross the blood-brain barrier and acts on EP3 and perhaps EP1 receptors on thermosensitive neurons, is NOT involved in normal thermoregulation
  • This triggers the hypothalamus to elevate body temperature by promoting an increase in heat generation and a decrease in heat loss
44
Q

Criteria for Graft-vs-host-disease?

A
  1. Graft must contain immunologically competent donor cells (T cells)
  2. Host is unable to reject/eliminate the donor cells of the graft: immunosuppressed so can’t stop the attack
  3. Host and graft must be antigenically different from each other (MHC)
45
Q

What is a Graft-vs-host-disease (GVHD)?

A

Donor T lymphocytes attack recipient tissues: respond to genetically determined proteins on recipient cells. These proteins are human leukocyte antigens (HLA) expressing peptides; HLA I and II are encoded by the MHC –> donor attacks recipient.

46
Q

Clinical scenarios in which GVHD can occur?

A
  1. Following an allogeneic stem cell transplant (most frequent kind) from bone marrow, peripheral blood or umbilical cord blood
  2. Syngeneic
  3. Autologous (plasma cell dyscrasia like multiple myeloma, lymphoma)
  4. Allogenic (AML, ALL): takes several months to plan
  5. Following solid organ transplant: rare because rejection is more prevalent
  6. Following a blood transfusion (transfusion-associated GVHD): rare, immunosuppressed host, can be prevented by irradiation of fresh blood products to inactivate T lymphs
47
Q

Patients at risk of developing GVHD?

A
  • HLA-mismatch between donor and recipient
  • Older age of the recipient
  • Immune-suppressed
  • Premature neonates, intrauterine transfusion recipients
  • Granulocyte transfusion recipients
  • Certain hematologic malignancies
  • Genetic polymorphisms in genes encoding cytokines and interleukins
  • Prior aGVHD
  • Donor alloimmunization
  • CMV seropositivity
48
Q

Clinical manifestations of GVHD?

A
  • Skin rash
  • Fever
  • Diarrhea and gut dysfunction
  • Hepatitis
  • Pancytopenia (bone marrow aplasia; chronic and more solid organs)
  • Anorexia, nausea, vomiting
  • Abdominal pain
49
Q

Treatment of GVHD?

A
  • Topical therapy only: grade I (skin stage < 2, mild skin rash)
  • Systemic steroids: > grade 2 (more severe rashes)
    Steroid refractory disease carries poor prognosis
50
Q

Treatement of asthma?

A
  • Anti-inflammatory (Steroids, inhaled or oral)
  • Anti-mediators (Antihistamines, antileukotrienes): Dupilumab binds
    specifically to the IL-4Rα subunit of the receptor complexes for IL-4 and IL-13, leading to inhibition of IL-4 and IL-13 signaling
  • Anti-IgE (Omalizumab): affects both early and late-phase asthma response
  • Anti-cytokines and anti-cytokine receptors (Multiple)

Bloc F - Defense (7 decks)

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