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ABBAS 1 Flashcards

1
Q

Features of the innate immunity

A
  • Provides early defence against infections by mediating RAPID initial responses against infections
  • Always present in healthy individuals
  • Blocks entry of microbes and rapidly eliminate those that do enter host tissue
  • Only recognise and react against microbes, do not react against non-infectious foreign substances
  • Enhance adaptive immune responses against infectious agents
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2
Q

Features of adaptive immunity

A

o Develops more slowly
o Mediates the later, more effective, defence against infections
o Stimulated by microbes that invade tissues
o Provide defence against infectious agents that can resist innate immunity
o Adaptive response only triggered if microbes or their antigens pass thru epithelial barriers and are delivered to lymphoid organs to be recognised by lymphocytes
o Cooperates with innate immunity: Ab binds to microbes (Antigen/Ag) – coated microbes avidly bind to and activate phagocytes (component of innate immunity) – ingest and destroy microbes

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3
Q

Innate immunity’s first line of defence

A

 Epithelial barriers
 Specialised cells
 Natural antibiotics
 Fxn: block microbe entry

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4
Q

Innate immunity’s second line of defence

A

 Phagocytes
 Natural Killer cells (NK cells)
 Complement system

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5
Q

Natural Killer cells

A

o Bone marrow derived lymphocytes of innate immune responses
o Kill microbe-infected cells
o Activate phagocytes by secreting Interferon-γ (IFN-γ)
o Do not express clonally distributed antigen receptors (Immunoglobulin for B cell; T cell receptor for T cell)
o Activation is regulated by a combination of cell surface stimulatory and inhibitory receptors – inhibitory receptors recognise self-MHC

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6
Q

Complement system

A

o System of serum and cell surface proteins
o Complement proteins generate effectors of both innate and adaptive immune responses
o 3 pathways of complement activation (differ in initiation method)
1. Classical pathway: activated by antigen-antibody complexes
2. Alternative pathway: microbial surfaces
3. Mannose-binding lectin pathway: plasma lectins tt bind to microbes
o Each pathway involves a cascade of proteolytic enzymes
 Generate inflammatory mediators and opsonins for phagocytosis by macrophages and neutrophils
 Lead to formation of a lytic complex that inserts in cell membranes

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7
Q

Adaptive immunity

A

2 types :
o Humoral immunity: Ab from B cells recognise antigens produced by extracellular microbes
o Cell-mediated immunity: T cells recognise antigens produced by intracellular microbes

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8
Q

Humoral Immunity

A

o Mediated by antibodies produced by B lymphocytes
o Ab secreted into circulation and mucosal fluids
o Ab neutralise and eliminate microbes and microbial toxins
 Outside of host cells
 In blood
 In lumens of mucosal organs eg. GIT, respiratory tract
o Fxn of Ab
 Stop microbes at mucosal surfaces and in blood from colonising host cells and connective tissues
 Prevent infections from getting established by blocking their ability to infect host cells
o Ab cannot gain access to microbes within infected cells -> cell-mediated immunity (T lymphocytes)
o Ab produced by B cells can recognise diff types of molecules (protein, carb, lipid)

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9
Q

Cell mediated immunity

A

o For intracellular microbes
o T lymphocytes
 Activate phagocytes to destroy microbes ingested by phagocytes into intracellular vesicles
 Kill infected host cells (harbouring infectious microbes in cytoplasm)
 Most T cells can only recognise protein Ag

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10
Q

Induced immunity

A
  • Active immunity

- Passive immunity

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11
Q

Induced active immunity

A

Induce immunity by infection or vaccination

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12
Q

Induced passive immunity

A

o Confer immunity onto naive individual (not previously exposed to microbe’s antigens) by transferring Ab or lymphocytes from an actively immunised person
o Useful for rapidly conferring immunity even before individual is able to mount an active response
o Does not induce long-lived resistance to infection
o Eg. Newborns are protected against infections thru acquiring Ab from mothers via placenta and milk since own immune system immature to respond to pathogen

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13
Q

Properties of adaptive

A
  1. Specificity and diversity
  2. Memory
  3. Clonal expansion
  4. Self-limited immune response
  5. Self tolerance
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14
Q
  1. Specificity and diversity
A

 Specific for many diff antigens
 Lymphocyte repertoire (total collection of lymphocyte specificities) is very diverse
 Lymphocytes express clonally distributed receptors for Ags
o Many different clones
o Each clone expresses an Ag receptor diff from the receptors of the other clones
 Clonal selection
o Clones of lymphocytes specific for diff Ags arise before encounter with Ags
o Each Ag elicits an immune response by selecting and activating lymphocytes of a specific clone
 At natural state, very few cells are specific for any 1 Ag
 To mount effective defence
o The few cells proliferate to generate a large number of cells
o Marked expansion of the pool of lymphocytes specific for any Ag subsequent to exposure to that Ag
o Positive feedback loops that amplify immune responses
o Selection mechanisms that preserve the most useful lymphocytes

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15
Q
  1. Memory of adaptive immunity system
A

 Larger and more effective responses to repeated exposures to the same Ag
 Primary immune response = response to the 1st exposure to Ag
o Mediated by naive lymphocytes (seeing Ag for the 1st time)
 Secondary immune response = subsequent encounters with the same Ag
o More rapid, larger, better able to eliminate Ag
o Memory lymphocytes (long-lived cells induced during primary immune response) activated
 Immunologic memory optimises ability of immune system to combat persistent and recurrent infections since each encounter generates more memory cells and activates previously generated memory cells
 Vaccines confer long-lasting protection against infections due to memory

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16
Q
  1. Clonal Expansion
A

 When lymphocytes are activated by Ag
o Undergo proliferation
o Generate many clonal progeny cells, all with same Ag specificity
 Ensures adaptive immunity keeps pace with rapidly proliferating microbes

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17
Q
  1. Self-limited immune response
A

 Immune response declines as infection is eliminated

 System returns to normal state

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18
Q
  1. Self-tolerance
A

 Does not react against host’s own potentially antigenic substances: self-antigens

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19
Q

Lymphocytes Features

A

 Express receptors for Ags
 Mediate immune response
 Innate: NK cells
 Adaptive: B and T cells
 Morphologically similar but heterogeneous in lineage, fxn and phenotype
 Distinguishable by surface proteins (monoclonal antibodies) – Cluster of Differentiation (CD)
 CD is recognised by a cluster or group of Abs

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20
Q

Maturation of lymphocytes

A

 Arise from stem cells in bone marrow
 Site of maturation (Generative lymphoid organs)
o B cell: bone marrow
o T cell: thymus
 Mature lymphocytes leave generative lymphoid organs, enter circulation and peripheral lymphoid organs
 10¹² lymphocytes in circulation and lymphoid tissues
 Ag-specific lymphocytes proliferate and differentiate into effector and memory cells upon contact of microbial Ags

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21
Q

B cells functions

A

o Express membrane forms of Abs – serve as receptors that recognise Ags
o Initiate process of activation of cells

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22
Q

T cells functions

A

o Ag receptors only recognise peptide fragments of protein Ags bound to specialised peptide display molecules – Major Histocompatibility Complex (MHC) molecules – on APCs
o Helper T cells (CD4+ T cells)
 Help B cells produce Abs
 Help phagocytes destroy ingested microbes
 Prevent or limit immune response (regulatory T lymphocytes)
o Cytotoxic/cytolytic T lymphocytes(CTLs) (CD8+ T cells)
 Lyse cells harbouring intracellular microbes

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23
Q

NK cells functions

A

o Kill infected host cells
o Do not express clonally distributed Ag receptors (unlike B and T cells)
o Rapidly attack infected cells

24
Q

Naive Lymphocytes functions

A

o Kill infected host cells
o Do not express clonally distributed Ag receptors (unlike B and T cells)
o Rapidly attack infected cells

25
Q

Effector cells functions

A

o Differentiated progeny of naive cells
o Can produce molecules to eliminate Ags
o B effector: plasma cells (Ab-secreting cells)
o T effectors
 CD4+ (Helper T cells): produce cytokines – activate B cells and macrophages
 CD8+ (CTLs): kill infected host cells
o Short-lived
o Die as Ag is eliminated
o Some may migrate to special anatomic sites and live for long, esp plasma cells

26
Q

Memory cells functions

A

o Survive for long time even in absence of Ag
o Frequency of cells increase with age due to exposure to environmental microbes
o Functionally inactive – do not perform effector fxns unless stimulated by Ag

27
Q

Antigen Presenting Cells (APCs)

A 
	Located in common portals of entry of microbes
o	Skin
o	GIT
o	Respiratory tract
	Action
o	Capture Ag
o	Transport Ag to peripheral lymphoid tissues
o	Display Ag to lymphocytes
28
Q

Antigen presentation to T lymphocytes by APC

A

Professional APCs (specialised cells tt display Ags to T cells and provide additional activating signals)

o Dendritic cells (DC)

  1. Capture protein Ag of microbes
  2. Transport Ag to regional lymph nodes
  3. Display parts of Ag for recognition by T lymphocytes

o Macrophages

  1. Phagocytose microbes that invade epithelium
  2. Present protein Ag to T cells

 Respond to microbes by producing surface and secreted proteins req tog with Ag to activate naive T lymphocytes to proliferate and diff into effector cells

29
Q

Antigen presentation to B lymphocytes by APC

A

o B cells may directly recognise Ags of microbes (released or on microbial surface)

o Macrophages lining lymphatic channels capture Ags, display to B cells

o Follicular dendritic cells (FDC)

  • Reside in germinal centres of lymphoid follicles in peripheral lymphoid organs
  • Display Ags that stimulate diff of B cells in follicles
  • Do not present Ag to T cells
30
Q

Effector cells - Leukocytes

A

Innate immunity

  1. Granulocytes
  2. Macrophages

Leukocytes directly recognise microbes, eliminate

31
Q

Macrophages

A

 Tissue-based phagocytic cell derived from blood monocytes
 Innate and adaptive immune responses
 Activated by
1. Microbial products eg. Endotoxin (aka lipopolysaccharide (LPS); component of bacterial cell wall; stimulates cytokine secretion, induce microbicidial activities of macrophages, stimulate exp of adhesion molecules for leukocytes on endothelium; contains lipid and carb components; recognised by Toll-Like Receptors (TRLs)/Pattern Recognition Receptors expressed by effector cells)
2. Molecules eg. CD40 ligand (CD40L)
3. T cell cytokines eg. Interferon-γ (IFN-γ)
 Different forms – microglia (CNS), Kupffer cells (liver), alveolar macrophages (lung), osteoclasts (bone)

32
Q

Lymphoid organs

A

Primary - Sites of T and B lymphocyte maturation
Eg. Bone marrow , Thymus , Foetal liver

Secondary - Where adaptive immune responses to microbes are initiated
Eg. Lymph nodes , Spleen , Mucosal and cutaneous immune system (Mucosal Associated Lymphoid Tissues - MALT)

33
Q

Functions of Secondary Lymphoid organs

A

o Optimise interaction of Ags, APCs and lymphocytes to promote devp of adaptive immune responses
o Anatomic organisation enables APCs to concentrate Ags in these organs
o Enable lymphocytes to locate and respond to Ags
o Bring helper T cells tog with B cells (both specific for the same Ag) together for productive interaction

34
Q

Lymph Nodes

A

o Lymph is drained from tissues and epithelia to the nodes via lymphatics
o Lymph enters via afferent lymphatic vessels and leaves via efferent
o Act as filters and slow down flow of lymph
o Dendritic cells pick up Ags of microbes from epithelia, transport to lymph nodes
o Microbial Ags that enter thru epithelia or colonise tissues become concentrated in draining lymph nodes
o Lymph-borne Ags
o As lymph passes thru lymph nodes, APCs in nodes sample Ags of microbes in lymph

o Lymphocytes in lymph can trap + phagocytose any foreign antigen

o B and T cells enter and leave via systemic circulation

o Diff. regions for B and T cells

o Medullary sinus à macrophages, direct to T cell or B cell area depending on response needed

35
Q

Spleen

A

o Filter Blood-borne Ags
o Blood entering spleen flows thru sinusoids (network of channels)

o White pulp = lymphoid tissue

o Distinct T and B cell zones

o Ags are trapped and concentrated by DC and macrophages in spleen

o Contains abundant phagocytes – ingest and destroy microbes in blood

o Afferent and efferent lymphatic vessels

o Arterial and venous connections

36
Q

Cutaneous and mucosal lymphoid systems

A

o Cutaneous lymphoid system: under skin epithelia, e.g. Langerhans cells (type of DC)
o Mucosal lymphoid system: under epithelia of GIT and respiratory tracts
o Mucosal lymphoid tissues
 Pharyngeal tissues
 Peyer’s patches (Intestine - large collection of lymphocytes – mainly B cells)
o Sites of immune responses to Ags that breach epithelia

37
Q

B cell organisations in Lymph Nodes

A

 Concentrated in follicles located around the periphery/cortex of each node
 Follicles contain FDCs (in close proximity to B cells)– activate B cells by secreting chemokines all the time, attracting B cells from blood into follicles; chemokines are chemoattractant cytokines – stimulate WBC movement, regulate WBC migration from blood to tissues; naive B cells express receptor for chemokines
 Germinal centre: central region of follicle if B cells have recently responded to Ag

38
Q

Anatomical organisation of

B lymphocytes in Spleen

A

Within Follicles

39
Q

Anatomical organisation of T lymphocytes in Lymph Nodes

A

 Concentrated outside, and adjacent to follicles, in the paracortex
 Paracortex contains DCs – present Ag to T cell

40
Q

Anatomical organisation of T lymphocytes in Spleen

A

 Concentrated in periarteriolar lymphoid sheaths surrounding small arterioles

41
Q

Naive T cells organisation

A

o Naive T cells express receptor CCR7 – recognise chemokines produced in regions of lymph nodes and spleen that contain T cells – recruit T cells from blood

42
Q

Upon activation of lymphocytes by microbial antigens

A

o Lymphocytes alter exp of chemokine receptors
o B and T cells migrate toward each other, meet at edge of follicles
o Helper T cells interact with and help B cells differentiate into Ab-producing cells
o Activated lymphocytes exit node via efferent lymphatic vessels, exit spleen via veins – go into circulation and distant sites of infection

43
Q

Lymphocytes recirculation and migration into tissues

A

 Naive lymphocytes constantly recirculate bt blood and peripheral lymphoid organs
 Activated by Ags to become effector cells
 Effector cells
o T cells: migrate to sites of infection
o B cells
- remain in lymphoid organs
- Do not migrate to sites of infection
- Secrete Abs which enter blood and find microbes and toxins in circulation

44
Q

Naive T cells recirculation

A

 Mature in thymus and leave to migrate to lymph nodes
 Enter lymph nodes thru high endothelial venules (HEVs), specialised postcapillary venules
 Express surface receptor L-selectin (protein involved in cell-cell adhesion) – binds to carb ligands expressed only on endothelial cells of HEVs
 Bind loosely to HEVs due to interaction of L-selectin with its ligand
 Chemokines produced in T cell zones of lymph nodes cause naive T cells to bind strongly to HEVs – migrate thru HEVs into region where Ags are displayed by DCs
 Scan surfaces of DCs searching for Ags in lymph node
 Recognise antigen, T cell transiently arrested on antigen-presenting DC, forms stable conjugate with APCs – activated T cell
 Most T cells in body circulate thru some lymph nodes at least once a day
 Likelihood of correct T cell finding its Ag increased in peripheral lymphoid organs since Ags are concentrated there – T cells circulate same areas
 Upon activation of T cells,
1. Cells reduce exp of adhesion molecules and chemokine receptors tt keep naive cells in lymph nodes
2. Increase expression of receptors for phospholid (sphingosine-1-phosphate) of which conc is higher in blood – cells are attracted out of nodes into circulation
3. Differentiated effector T cells thus leave nodes and enter circulation

45
Q

B lymphocytes circulation

A

o Enter lymph nodes thru HEVs
o Upon Ag contact differentiated progeny
 Remain in lymph nodes
 Migrate to bone marrow

46
Q

How does epithelial serve as first line of defence in innate immunity?

A
  1. Physical and functional barriers to infection
  2. Impede entry of microbes
  3. Interfere with growth of microbes thru production of natural antimicrobial agents
47
Q

Phagocytes

A
  1. Neutrophils and macrophages
  2. Ingest microbes into vesicles
  3. Destroy them by producing microbicidal substances in vesicles
48
Q

Cytokines

A
  1. Soluble proteins secreted by macrophages, DCs and NK cells
  2. Stimulate inflammation and lymphocyte response
49
Q

Development of response

A
  1. Capture and display of microbial Ags
  2. Cell-mediated immunity: activation of T cells and elimination of cell-associated microbes
  3. Humoral immunity: activation of B cells and elimination of extracellular microbes
50
Q

Adaptive step 1. Capture and display of microbial antigens

A

 Microbes and protein Ags captured by DCs resident in epithelia
 Cell-bound Ags transported to draining lymph nodes
 Protein Ags processed in DCs – generate peptides – displayed on APC surface bound to Major Histocompatibility Complexes (MHCs)
 Naive T cells recognise peptide-MHC complexes
 B cells recognise polysaccharide, protein and non-protein Ags
 T cells only recognise protein Ags
 Innate immune response
o DCs presenting Ags to naive T cells express costimulators and secrete cytokines – stimulate proliferation and differentiation of T lymphocytes
o Activate complement system – generate cleavage products of complement proteins tt enhance proliferation and diff of B lymphocytes
 Antigen (signal 1) and molecules produced from innate immune response (signal 2) cooperate to activate Ag-specific lymphocytes-> Adaptive immune response
 Signal 2 is only triggered by microbes, thus ensuring tt adaptive immune response is induced by microbes, not harmless substances
 Ag and costimulator receptors engaged -> signals generated in lymphocytes -> transcription of genes that encode
o Cytokines
o Cytokine receptors
o Effector molecules
o Proteins tt control cell cycling

51
Q

Major Histocompatibility protein (MHC)

A

o Heterodimeric membrane protein
o Serves as a peptide display molecule for recognition by T lymphocytes
o 2 classes
1. MHC Class I: present on all nucleated cells (thus absent in RBC), bind peptides from cytosolic proteins, recognised by CD8+ T cells

  • Present peptides derived from degradation of viral and other cytosolic proteins
  • Degradation of proteins is mediated by cytosolic and nuclear proteasomes (protein complexes that use proteases to degrade unneeded proteins)
  1. MHC Class II: restricted to professional APCs, macrophages, B lymphocytes; bind peptides from endocytosed proteins, recognised by CD4+ T cells
    Activated T helper cells produce cytokines to activate other cells such as B cells
  • Bind to peptides that are derived from proteins degraded in endocytic pathway i.e. phagocytosed pathogens that are degraded
52
Q

Adaptive step 2. Cell-mediated immunity

A

 Naive T cells
o Activated by Ag and costimulators in lymphoid organs
o Secrete cytokine growth factors and respond to cytokines secreted by APCs

 Ag + costimulation + cytokine -> proliferation of T cells and differentiation into effector T cells

 Naive CD4+ T cells -> Helper T cells
o Produce cytokines
o Express cell surface molecules tt bind to receptors on B cells and macrophages -> promote Ab production and macrophage killing of ingested microbes
o Recruit and activate neutrophils (polymorphonuclear leukocyte (PMN), most abundant WBC, recruited to inflammatory sites, phagocytoses and digests microbes enzymatically) -> destroy microbes

 Naive CD8+ T cells -> CTLs
o Directly kill cells harbouring microbes in cytoplasm
o Usually viruses that escape from phagocytic vesicles into cytoplasm where they are inaccessible to killing machinery of phagocytes (confined to vesicles)

53
Q

Adaptive step 3. Humoral Immunity

A

 Activated B cells proliferate and differentiate into plasma cells -> secrete Abs
 Many polysaccharide and lipid Ags have multiple identical antigenic determinants/epitopes (specific portion of a macromolecular Ag to which Ab binds; for T cell, epitope is peptide portion tt binds to MHC for TCR recognition)
 Epitopes able to engage many Ag receptor molecules on each B cell -> initiate B cell activation
 Globular protein Ags unable to bind to many Ag receptors -> full response of B cells to protein Ag requires CD4+ helper T cells
 B cells ingest protein Ags -> degrade Ags -> display peptides bound to MHC for recognition by helper T cells
 Helper T cells express cytokines and cell surface proteins – work tog to activate B cells
 Each B cell secretes Abs tt have the same Ag-binding site as the BCR that first recognised Ag
 Polysaccharides and lipids stimulate secretion of IgM
 Protein Ags stimulate helper T cells -> induce production of IgG, IgA and IgE
 Heavy chain class (isotype) switching
 Affinity maturation

54
Q

Heavy chain class switching

A

o Process by which a B cell changes the isotype of Abs it produces, but with same Ab specificity
o Change from IgM to IgG, IgA or IgE without changing Ab specificity
o Regulated by helper T cell cytokines and CD40 ligand
o Involves recombination of heavy chain VDJ segments with downstream constant region gene segments
o Provide plasticity in Ab response, enable Abs to serve many fxns

55
Q

Affinity Maturation

A

o Process tt leads to increased affinity of Abs for a protein Ag as a humoral response progresses
o Results from somatic mutation of Ig genes followed by selective survival of B cells producing highest affinity Abs
o Helper T cells help in Ab production with higher affinity for Ag
o Increases quality of humoral immune response

56
Q

Decline of immune response and immunological memory

A

 Most effector lymphocytes induced by pathogen die by apoptosis after microbe is eliminated -> homeostasis
 Microbes provide essential stimuli for lymphocyte survival and activation
 Effector cells are short-lived
 As stimuli eliminated, activated lymphocytes not kept alive
 Long-lived memory cells
o Can survive for years after infection
o Expanded pool of Ag-specific lymphocytes (more than Ag-specific naive cells present before encounter with Ag)
o Respond faster and more effectively than naive cells
o Goal of vaccination: generate memory cells

Medicine (8 decks)

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