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Foundations of Health and Disease > Infection And Immunity > Flashcards

Infection And Immunity Flashcards

1
Q

Define immunity

A

The ability of an organism to defend itself: 1. Infectious agents 2. Foreign cells and proteins 3. Catastrophic cell dysfunction (e.g., cancer)

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2
Q

When and how does immunodeficiency occur

A

Immunodeficiency results when immunity fails; it can be the result of: -Genetic Inheritance (e..g, severe combined immune deficiency SCID) -Acquired during life (e.g., acquired immune deficiency syndrome AIDS)

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3
Q

Define Immune tolerance

A

• Tolerance is defined as a state of immunoglocial non-reactivity to an antigen. • The immune system has powerful weapons at its disposal to attack and destroy pathogens and infected tissues, and it is vial that any attack is initiated because it is essential to survival • Many potential antigens are not harmful: -Our own cells and tissues (‘self’ antigens) -Harmless environmental antigens (food sources, pollen) -Commensalism organisms (e..g, skin and gut flora) • An immune response to self tissue- a breakdown of tolerance- results in autoimmune disease.

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4
Q

Differences between innate and adaptive immunity.

A

Innate immunity responds rapidly to an infection, but the lac of ability to adapt may sometimes result in failure. Adaptive immunity takes time to develop, but the ability to recognise a vast variety of antigens makes it potent. In addition, adaptive immunity exhibits a memory function that kicks in quickly if a pathogen is encountered again later in life.

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5
Q

List the different lymphoid tissues

A

Lymph nodes- oviod or round structures found in lymphatic vessels, contain resident lymphocytes and macrophages, cells which neutralise pathogens and clear debris Red bone marrow- site of production of all blood cells (including B and T cells) Spleen- emergency blood store, blood is cleansed of pathogens and debris. Thymus- site of T-lymphocytes maturation.

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6
Q

Define epitope

A

Site of an antigen where the antibody binds to

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7
Q

Barrier systems in innate immunity

A

Skin- antimicrobial peptides, fatty acids in sebum Mouth and upper alimentary canal- enzymes, antimicrobial peptides, and sweeping of surface by directional flow of fluid toward stomach Stomach- low pH, digestive enzymes, antimicrobial peptides, fluid flow towards intestine Small intestine- Digestive enzymes, antimicrobial peptides, fluid flow to large intestine Large intestine- Normal intestinal flora compete with invading microbes, fluid/faeces expelled from rectum Airway and lungs- Cilia sweep mucous outward, coughing, sneezing expel mucous, macrophages in alveoli of lungs

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8
Q

Myeloid and Lymphoid leukocyte lineages

A

Image

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9
Q

Define HEVs

A

High endothelial Venules (HEVs) are the site in lymph nodes where lymphocytes cross from blood to the lymphatic system.

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10
Q

What is the purpose of lymphocyte recirculation

A
  1. The purpose of continual lymphocyte recirculation allows maximum number of antigenically committed lymphocytes to encounter and interact with antigen. 2. An individual lymphocyte may make a complete circuit around the system 1 to 2 times a day 3. Approx 1 in 100,000 lymphocytes will bind to a particular antigen, so it is essential that each lymphocyte travels widely in the body to stand a chance of detecting the presence of antigen. 4. Before a lymphocyte can enter inflamed tissue or peripheral lymphoid organs, it must adhere to and penetrate the layer of endothelial cells lining the walls of blood vessels.
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11
Q

Leukocyte communication

A
  1. Autocrine 2. Paracrine 3. Endocrine They communicate using small soluble messaging proteins known as cytokines or chemokines that bind to receptors on the target cell to trigger signalling transduction cascades that lead changes in gene expression and therefore, cell function.
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12
Q

The inflammatory response

A
  1. Tissue damage causes release of vasocactive and chemotactic factors that trigger a local increase in blood flow and capillary permeability. 2. Permeable capillaries allow an influx of fluid (exudate) and cells. 3. Phagocytes migrate to site of inflammation (chemotaxis). 4. Phagocytes and antibacterial exudate destroy bacteria.
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13
Q

Define antibody

A
  1. Antibodies are glycoproteins with a min molecular weight of 150kDa. 2. Each antibody will bind to a single specific antigen. 3. Through its lifetime, each individual B lymphocyte produces antibodies that bind to the same antigen, but the exact structure of the antibody changes over time in terms of the scaffold on which the antigen binding ‘head’ sits. 4. There are billions of different B lymphocytes in the human body, and each is theoretically capable of producing an antibody to a different antigen.
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14
Q

Antibody structure

A

In a non activated B cell, the antibody includes an additional transmembrane domain that anchors it on the surface of the B cell. In this format, it is known as a B Cell Receptor (BCR). Once the BCR is activated by antigen cross linking and additional cytokines-mediated stimulation by T helper cells, the mature B cell undergoes BCR gene rearrangements that allow the secretion of the antigen binding site remains identical throughout. The Variable (V) and Constant (C) domains of the IgG Heavy (H) and Light (L) chains are depicted in different colours. Each L chain has one C domain whilst each H chain has three C domains.

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15
Q

Clonal expansion

A
  • Each T cell and B cell expresses its own antigen receptor.
  • Activation required cell leads to the production of clones with the same antigen-binding capability
  • Stimulation of growth factors such as IL2
  • Either of these binding events alone can result in an ability to subsequently be activated (anergy), or even cell death by apoptosis.
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16
Q

CD4+ and CD8+

A

CD4+: Adhesion molecule that binds to Class II MHC molecules; signal transduction- T helper cells

CD8+:Adhesion molecule that binds to Class I MHC molecules; signal transduction- cytotoxic T cells

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17
Q

Different kinds of Antibodies/Immunoglobulins

A

Valency:

IgG, IgD, IgE: 1

IgM: 5 (pentameric structure) 5 individual antibody molecules are linked together by the J achain. This gives the molecule 10 binding sites, so even if the affinity for antigen is not yet fully developed, the avidity effect compensates for this.

IgA: 1/2 (dimer) two individual antibody molecules are linked together by a J chain and the secretory piece that protects from proteolysis and facilitates secretion across mucous membranes.

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18
Q

Affinity and Avidity

A

Affinity and avidity are both measures of binding strength. While affinity is the measure of the binding strength at a single binding site, avidity is a measure of the total binding strength.

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19
Q

Cells of the innate immune system

A

Macrophage: phagocytic, highly migratory, professional APC

Neutrophil: highly abundant and migratory; coordinates inflammatory response.

Eosinophil: involved in host defence against nematodes and other parasites.

Basophil- involved in host defences against multicellular parasites

Dendritic cells- the most adept of the family of APCs

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20
Q

PAMPs

A

Pathogen Associated Molecular Patters (PAMPs). Pattern Recongnition Receptors (PRR) in innate immunity detect antigens non-specifically using receptors for PAMPs, i.e., Toll-like receptors. PMAPs are molecular structures that occur in microbes, but not humans. E.g., lipopolysaccharide from the outer membrane of a G- bacteria, peptidoglycan found in G+ cell wall.

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21
Q

Contrasting PRRs and Adaptive response receptors

A
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22
Q

Soluble factors that play a role in innate immunity (3)

A
  1. Complement: -a family of plasma proteins that activate each other: the complement cascade -capable of destabilizing the membranes of invading bacteria -coats invading bacteria, marking them for destruction by antibodies -attracts phagocytes to the site of the infection
  2. Lysozyme: - hydrologic enzyme present in saliva, tears -destroys the bacterial cell wall
  3. Cytokines (including chemokines that attract cells to the site of infection) e.g., interferon, a glycoprotein that interferes with viral replication
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23
Q

How does somatic recombination contribute to antibody diversity?

A
  • The chains of the antibody molecule are put together by splicing (V), diversity (D), joining (J), and constant (C) gene segments together.
  • the H chain is formed from V, D, J and C whilst the L chain lacks D.
  • the reaction requires recombination signal sequences and activation enzymes including RAG-1/2 and epigenetic changes (do not affect the nucleotide sequence) to the DNA structure that include changes to methylation and acteylation.
  • this generates a huge repertoire of available antibodies allowing the immune system to tackle the many pathogenic threats we face in a lifetime.
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24
Q

How does a B cell mature?

A

B cells express a receptor that binds to an antigen on the target pathogen and this leads to the secretion of soluble antibodies to neutralize the pathogen. Memory cells are also produced. These have very long lifespans and can react quickly if the pathogen is ever encountered again. Affinity maturation involves minor changes in the amino acid sequence of the variable domain the mature B cell once it encounters antigen for the first time.

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25
Q

How do primary and secondary responses differ?

A
  • primary phase: the first isotopes to be produced by a B cell are IgD and IgM, and then class switching results in the generation of IgG, which is the main mature antibody form. A switchback from IgG to IgM is not then possible. The switching affects the constant domain, and therefore the antibody retains an affinity for the same antigen but interacts with different effector molecules.
  • during the secondary phase, less IgM is produced and a lot more IgG is produced.
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26
Q

Comparison of primary and secondary antibody responses

A
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27
Q

T Helper Cells

A

Secrete hormones known as cytokines (also known as lymphokines) that bind to receptors on B cells and T cells to stimulate their activity.

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28
Q

T Suppressor

A

Secrete hormones that bind to receptors on other immune cells to terminate their activity, thus suppressing immune responses that are no longer needed.

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29
Q

T Memory

A

Persist for life in a semi-dormant state, but rapidly re-activated on a second exposure to the antigen (pathogen) they are specific for. Bypass the need for the primary immune response on second infection

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30
Q

How do cytotoxic T cells respond to antigens

A
  • Cytotoxic T cells respond to antigens presented in MHC Class I context
  • Once the peptide is loaded into the MHC Class I complex and presented on the surface of an infected cell, it engages with the T cell receptors on a passing cytotoxic CD8+ T cell (CTL)
  • The CD8+ molecule on the surface of the CTL simultaneously ‘double checks’ that the peptide is presented correctly by recognizing that the MHC Class I molecule is from a matched allele
  • The CTL will only kill the target cell once these engagements are complete.
31
Q

How do T helper cells respond to antigens?

A
  • Helper T cells responds to antigen presented in MHC Class II contect
  • Once the peptide is loaded onto the MHC Class II complex and presented on the surface of a professional APC, it engages with the T cell receptor on a passing CD4+ helper T cell.
  • The helper T cell ‘double checks’ the identity of the presenting cell before it becomes activated to secrete molecular messengers (cytokines) that further promote immune response.
32
Q

Contrasting MHC Class I and MHC Class II

A
33
Q

Endogenous

A

-The endogenous pathways evolved to deal with intracellular infections (largely viruses). The vast majority of vertebrae nucleated body cells are capable of expressing MHC Class I and cytotoxic peptides are presented constitutively, not just during infection. This means that the vast majority of peptides presented in the Class I context are self-derived and will not trigger an immune response.

34
Q

Exogenous pathway

A

The exogenous pathway evolved to deal with extracellular infections (non-viral pathogens). Only a select group of immune cells are capable of Class II MHC presentations, including dendritic cells, macrophages, and B cells.

35
Q

T Cell Receptor rearrangement

A
  • The number of potential antigen shapes that need to be recognized by T cell receptors is huge, and it would not be possible for all of this to be encoded in the germline (genome).
  • T cell receptors include alpha and beta subunits, each of which is made by randomly combining V/J/C (alpha) or V/D/J/C (beta) regions; the largest diversity is in the V regions, and all three mRNA frames can be used during translation.
  • Unlike B cells, there is not an affinity maturation in T cells, nor is there a substitution of C domains during the immune response.
36
Q

Contrasting CD4+ and CD8+ T cells

A
37
Q

Contrasting B cells and T cells

A
38
Q

Comparison of Innate and Adaptative Immunity

A
39
Q

What does tissue growth result from?

A
  • Increase in cell number by mitotic division
  • increase in cell size (auxesis)
  • increase in extracellular tissue (accretionary mechanism)
  • combination of the above
40
Q
A
41
Q

Physiological Cell turnover during development

A

Fetal: rapid growth and apoptosis

Childhood/adolescence: rapid growth of most tissues with atrophy in some (thymus)

Adults: -many mature tissues/cells loose proliferation ability

-some tissues retain active proliferation/turnover to meet the specific function: skin, gut, and respiratory lining (mucosa), blood cells.

42
Q

Labile

A

Continuously proliferate, have a short lifespan and a rapid turnover: blood cells, endothelial cells

43
Q

Stable

A

have good regenerative ability but would normally have a low cell turnover: hepatocytes (quiescent tissues or facultative dividers)

44
Q

Permanent cells

A

have have limited or none regenerative ability: cardiomyocytes, neurons (terminally differentiated cells)

45
Q

The cell cycle

A
46
Q

Response to injury

A
47
Q

Hypertrophy

A
  • increase in cell size
  • the only adaptative response seen in permanent cells
  • lead to increase in tissue/organ size and function

includes muscle hypertrophy, physiological hypertrophy, pathological hypertrophy

48
Q

Hyperplasia

A
  • increase in cell number
  • requires cells to be able to divide (labile or stable cells)
  • often hyperplasia and hypertrophy occur together
  • physiological hyperplasia: -hormonal hyperplasia which increased the functional capacity (breast feeding), compensatory hyperplasia when tissue was lost (partial liver resection).

–pathological hyperplasia: usually excess hormonal stimulation of the cells- male breast enlargement in excess of androgens or steroids, endometrial hyperplasia due to excess estrogen stimulation -prostatic hyperplasia due to hormonal disbalance, dihydrotestosterone or oestrogen

49
Q

Atrophy

A
  • Reduction in the cell size and number
  • Related to decrease the function of the tissue organ
  • Often hormonally regulated.
  • physiological atrophy: testicular atrophy, ovarian atrophy, breast atrophy, endometrial uterine lining, atrophy due to reduction in hormonal stimulation in older age.
  • pathogical atrophy: denervation of muscle (trauma, neurological disorders), muscle atrophy in immobilisation, vascular atrophy of the brain (ageing), malnutrition/starvation, pressure atrophy due to adjacent mass effect (tumour)
50
Q

Metaplasia

A
  • reversible change where one differentiated cell type or tissue is replaced by another differentiated cell/tissue
  • often seen in the epithelium
  • mechanism: stem cells differentiate along a different pathway due to change in the local microenvironment, it’s not a change of phenotype/morphology of the differentiated cell.
  • pathological metaplasia: -bronchial metaplasia: replacement of bronchial ciliated columnar epithelium by stratified squamous epithelium in response to smoking -Barrett’s oesophagus: replacement of oesophageal stratified squamoud epithelium by columnar epithelium, including intestinal goblet cells.
51
Q

Cell death. What are the two pathways to cell death?

A
  • If a cell cannot recover from injury it dies.

Two principal pathways of cellular death which differ in morphology, mechanism and role in disease:

  • Apoptosis: programmed cell death: physiological and pathological
  • Necrosis: pathological
52
Q

Contrast Necrosis and Apoptosis

A
53
Q

Cell Necrosis

A
  • ATP depletion
  • Mitochondiral damage
  • Influx of calcium
  • Accumulation of oxygen radicals
  • Increased membrane permeability
  • DNA and protein damage
  • Coagulative necrosis: shape and architecture are preserved for some time
  • Liquefaction necrosis: liquified, viscous, soft lesion, bacterial infection in brain
  • Caseous necrosis: cheese-like appearance , usually mycobacterial
54
Q

Apoptosis

A
  • pathway of programmed cell death
  • activation of intracellular enzymes to degrade DNA and proteins
  • Cell membrane remains intact but attracts phagocytes
  • Four phases: induction, effector, degradation, phagocytosis
  • Physiological apoptosis: -embryogenesis, involution of hormone-dependent tissues after hormone withdrawal (menustral cycle), high turnover tissues (intestinal epithelium), elimination of self reactive/autoimmune lymphocytes, destruction of inflammatory cells.

pathological apoptosis: DNA damage of any kind usually triggers apoptosis, accumulation of abnormal proteins, some infections (e.g., HIV), duct obstruction may causes apoptosis (kidney and pancreas)

55
Q

Autophagy

A
  • Associated cell death
  • the cell breaks down its own contents as a survival mechanism in nutrient deprivation
  • regulated by autophagy genes
  • overlap with apoptosis
  • may be a defence against neoplasia
56
Q

Define inflammation

A

Inflammation is the local response of living tissue to injury from any agent which could be microbial, immunological, physical or chemical

57
Q

Signs and Symptoms of Inflammation

A

Symptoms: redness, swelling, heat, pain

Clinical signs:

  • RUBOR: redness
  • TUMOR: swelling
  • CALOR: heat/warm
  • DOLOR: pain and functio laesa (loss of function)
58
Q

Major phases of the inflammation response process

A
  1. Vascular phase: increased blood flow, dilation of small blood vessels and increased movement of fluid from blood to tissue producing swelling/oedema
  2. Neutrophils Phase (initial appearance of neutrophils first type of leucocyte at the site of injury)
  3. Macrophage Phase (later appearance of macrophages second type of leucocyte)
59
Q

Neutrophil phase in inflammation response

A
  1. Neutrophils are -abundant in circulation -stored/released from bone marrow -multi-lobed nucelate -granulocytes
  2. Neutrophils destroy -granule release: array of bactericidal proteins -engulf (phagocytose) microbes: intracellular killing mechanisms -apoptose -NET
  3. Neutrophils signal: -other neutrophils -macrophages
60
Q

Macrophages

A
  1. Macrophages are -few in circulation -some resident in tissues (specialised for detection of injury) -mono-nucleate -agranular
  2. Macrophages function: -second line microbe destruction -phagocytosis, less efficient killer -clear debris, dead neutrophils, dead microbes ‘scavenge’ -M1/M2 phenotypes
  3. Macrophages signal: -other cell types to start healing -other immune cells as part of immunity (antigen presenting)
61
Q

The phases through which the circulating leucocytes attach to the endothelial cells and their migration

A
  1. Margination:The main immune cells involved in acute inflammation are neutrophils. The stasis of circulation allows neutrophils to line up along the endothelium near the site of injury, known as margination.
  2. Rolling: In inflammation, neutrophils roll along the endothelial wall of postcapillary venules and sample inflammatory signals. Rolling cells that do not reach the activation threshold detach from the endothelium and are released back into the circulation.
  3. Adhesion to endothelium: 1. Selectins 2. Integrins 3. The immunoglobulin family molecules 4. Mucin like glycoproteins
62
Q

Adhesion to endothelium in inflammation

Selectins

A
  1. Selectins cause mainly loose adhesion
    - E selectin: confined to Endothelium
    - P selectin: present in endothelium and platelets
    - L selectin- expressed on most Leucocyte and endothelium
63
Q

Adhesion to endothelium in inflammation:

Integrins

A
  • transmembrane glycoproteins
  • cause firm adhesion
  • expressed on many cell types and bind to ligands on endothelial cells and leucocytes
64
Q

Adhesion to endothelium in inflammation:

The immunoglobulin family molecules

A
  • ICAM-1 (intercellular adhesion molecule 1)
  • VCAM-1 (vascular cell adhesion molecule 1)
  • PECAM-1 (platelet endothelial cell adhesion molecule 1)
  • induced by TNF and IL-4.
  • mainly involved in transmigration
65
Q

Adhesion to endothelium in inflammation

Mucin like glycoproteins

A

These glycoproteins are found in the extracellular matrix and on cell surfaces.

66
Q

Chemotaxis

A

-After extravasation, leucocytes emigrate in tissues toward the site of injury by a process called chemotaxis, as locomotion oriented along a chemical gradient.

Chemoattractants: Complement protein C5a, Leukotriene and cerain chemokines like MCP (macrophage chemoattractant protein)

67
Q

Three stages in Phagocytosis (neutrophils and macrophages):

A
  1. Recognition and attachment of the particle to be ingested by the leucocyte
  2. Engulfment, with subsequent formation of a phagocytosis vacuole
  3. Killing or Degradation of the ingested material
68
Q

How do phagocytes recognise pathogens?

A

Opsonisation is the process of coating a pathogen to target it for phagocytosis by opsonins which could include antibodies (IgG) or a component of the Complement System (C3). These opsonins are recognized by receptors on phagocytes.

69
Q

Oxygen-dependent mechanism vs Oxygen-independent mechanism for Intracellular killing.

A
  1. Oxygen-dependent mechanism: -highly effective -neutrophils only MPO-(HOCI) -peroxynitrite (superoxide radical and nitric oxide) in macrophages
  2. Oxygen-independent mechanism: Granules containing multiple bactericidal proteins -Lysozymes containing enzymes -Neutrophils and macrophages.
70
Q

Morphological patterns:

Serous

A

Watery, low protein secretion

71
Q

Fibrinous

A

Shaggy, high protein, coagulated secretion

72
Q

Morphological patterns:

Purulent (suppurative)

A

Offensive, thick pus secreted

73
Q
A

Foundations of Health and Disease (6 decks)

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