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AAPathology > Immune cells > Flashcards

Immune cells Flashcards

(55 cards)

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1
Q

Neutrophil histological features

A

Distinctive cytoplasmic granules visible in EM.

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2
Q

Stem cell development

A

Cells of blood arise from either myeloid or lymphoid stem-derived haematopoietic stem cells. Most blood cells exist in plasma or lymph but some sequestered into specific tissues which may then occasionall recirculate.

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3
Q

Mast cells histological features

A

Stain blue due to granules containing heparin and histamine. Present in all tissues, generally close to blood vessels and mucosae.

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4
Q

Monocytes features

A

Present in blood, they are CD14 positive and last 1-2 days in the circulation.

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5
Q

Macrophage features

A

Present in tissues. CD68 positive and last between weeks, months and years. ?different derivation from the yolk sac. Dominate secretory landscape within the tissue.

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6
Q

Roles of macrophages

A

Tissue maintenance: homeostasis, remodelling (partic in development), apoptotic cell clearance and tissue repair.
Immune regulation: of acute and chronic inflammation, professional APCs - presenting antigen on MHC II and produce cytokines and growth factors.
Pathogen control: are the guard cells initiating acute inflammation, phagocytose pathogens, and kill pathogens using ROS and RNS. Phagocytose microorganisms in a nonspecific fashion although are made more efficient by PRRs or receptors for complement fragments.

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7
Q

Process of leukocyte recruitment

A
  1. margination
  2. Rolling
  3. Activation
  4. Tight adhesion
  5. Extravasation
    6 Chemotaxis
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8
Q

Neutrophil granules

A

Many dangerous substances contained within granules, which are mobilised to fuse either with a phagosome membrane or cell surface membrane to release contents to kill pathogens. Some directly or indirectly kill bacteria - eg LL-37, BPI, lysozyme, neutrophil elastase and lactoferrin.

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9
Q

LL-37

A

Induces transmembrane pore formation - we used in that path experiment…

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10
Q

Production of ROS

A

NADPH oxidase complex assembles on membrane (incorporated membrane of vesicle?) and begins production of superoxide then progresses to hydrogen peroxide , and can react with NO to form peroxynitrite. Hydrogen peroxide can also react with MPO to make hydrophalous acid…

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11
Q

NETosis

A

Active form of cell death which releases decondensed chromatin into the extracellular space. Contains histones and antimicrobial proteins to then trap and kill microbes in high concentration.

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12
Q

Weapons of the adaptive immune systems

A

Immunoglobulin, cytotoxic T lymphocytes and natural killer cells.

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13
Q

Recognition system based on PAMPs

A

Cannot be misconstrued, little opportunity of recognising self as foreign. Specturm of carbohydrate and nucleic acid species is limited so the diversity of receptors required to detect them is also low. Receptors are germ line encoded and highly conserved.

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14
Q

Adaptive immune system recognition

A

Proteins are infinitely diverse (about 10^9 possibilities) and so complementary diversity of receptors is required.
Significant likelihood of cross-reactivity to eukaryotic homologue proteins.
Hence antigen recognition is required to be very specific and precise to limit collateral damage to tissues.

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15
Q

Immunoglobulins which activate complement

A

IgG and IgM

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16
Q

IgE

A

Very specific activity in mast cell and basophil degranulation

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17
Q

B cells

A

Produce only one antibody, so have a ver particular specificity. Binding of the correct antigen (along with other signals) is a potent stimulus for proliferative burst. Many clonal B cells produced and so antibody for that antigen.

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18
Q

Characteristics of the adaptive immune response

A

Kinetics measured in days rather than minutes.
REsponse is exquisitely specific and exploits the vulnerabilities of the individual target microorganism.
Capactity for immunological memory, facilitating more rapid (no lag phase) and effective response on second exposure.
Capacity for immunological tolerance to limit deletrious responses to innocuous substances or self components.

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19
Q

Immunoglobulin structure

A

Highly specific made up of two light and two heavy chains bound by disufide bonds. FAb (fragment antigen binding) portion at top end confers specificity. Physical attachment to antigens at complementarity determining region.
Hinge region then separates from Fc portion = recruitment of effector functions.

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20
Q

Antibody possible effects

A

Opsonisation
Complement fixation
Neutralisation

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21
Q

Heavy chain components

A

Variable domain, constant region, hinge region, two more constant domains

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22
Q

Light chains components

A

One variable and one constant domain

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23
Q

Fab region

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A

‘Arms’ of the Y shaped immunoglobulin. Tips of arms are made up of V domains, and three beta strand loops from the ends of the light and heavy chain are responsible for antigen binding = complementarity determining region.

24
Q

Fc region

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A

Two constant domains, able to bind to Fc receptors on the surfaces of other immune cells. Can mediate phagocytosis, or bind to complement proteins, or to specialised Fc receptors on oesinophils and mast cells to trigger degranulation.

25
Classical complement pathway
C1 binds to Fc portion of IgG or IgM that have opsonised the antigen.
26
Class-switching
All B cells start out by producing IgM antibodies, and then class switch to produce other antibodies, dependent on cytokine signalling. C segment in heavy chain determines class, so C segments will be cut out, leaving Fab the same in class switching. Carried out by VDJ recombinase which randomly selects genes and cuts out stretches of DNA in between.
27
IgG features
About 80% of total antibody in plasma. Located both intra and extravascular. Do activate complement, some bind to phagocytes and macrophages. Pass via placenta to fetus/
28
IgM features
9% of antibody proportion in plasma. Only intravascular. Structure is pentameric (although monomeric when acting as B cell receptor). First to be produced so have high avidity and low affinity. Strong complement activation, no binding to phagocytes or macrophages.
29
IgA features
13% total in plasma. Located on secretory surfaces, and present in secretions including milk/colustrum. Dimeric structure. Does not activate complement or neutrophils, low affinity phagocyte binding.
30
IgD
B-cell surface receptor
31
IgE
About 1% total antibody abundance, present on mast cells, basophils and insecretions. Main role in high affinity activation of basophils and mast cells.
32
Diversity of Ig
Dependent on selection of gene segments expressed. Possibilities light: 30 V, 4 J and 1 C. Heavy 100-1000 V, 20 D, 4 J, and 8 C. Multiple copies of VDJC are randomly recombined.
33
Other generation of fiversity
VDJC randomly combined. D regions transcribed in multiple reading frames Imprecise joining occurs About 10^16 possible antibodies.
34
Somatic hypermutation
Mutation rate in VDJ reions is very high, so affinity for antigen constantly changed by accumulation of mutations. Driven by activation induced deaminase (AID), and error prone DNA pathways. Competition for antigen so higher affinity Igs will be selected for and survive with increasing frequency = affinity maturation over time.
35
Problems with phagocytosis
-Regurgitation and frustrated phagocytosis -> some components are exocytosed - Surface phagocytosis of tissues Evasion of phagocytosis as bacteria evolve escape mechanisms
36
Stages of phagocytosis
1. Particle enveloped 2. NADPH oxidase complex assembled 3. Early phagosome 4. Fuse with lysosome 5. Phagolysosomal digestion
37
Oxygen-dependent antibacterial mechanisms
NADPH oxidase complex reduces superoxide radical O2-. Then Hydrogen peroxide and O2- are used to generate bactericidal molecules. May be combined with halides by myeloperoxidase to form hypochlorite = bleach.
38
Oxygen-independent antibactericidal mechanisms
Phagocyte many enzymes produced in phagosome to break down microorganisms. eg proteases, nucleases, lysozyme, cationic proteins, lactoferrins etc. One type of defensin = antimicrobial peptides (AMPs) eg LL-37 = can kill Gram - and + bacteria in vitro via direct interaction. Eg positively charged amino acid residues and hydrophobic can interact and perforate membrane. Equaally active against antibiotic resistant strains.
39
Reactive nitrogen species
NO generated by the phagocyte enzyme inducible nitric oxide synthase (iNOS). iNOS synthesis increased in the presence of inflammatory markers. And high NO levels can kill viruses, bacteria, fungi, helminths and tumour viruses.
40
NETs
= Neutrophil Extracellular Traps. Dying neutrophils extrude nuclear material of Dna and histones producing a mesh substance to which antimicrobial proteins are tightly bound. Very effective containment of bacteria and large particles whilst causing minimum damage to host cells.. Some bacteria can evade NET killing, eg by production of bacterial catalase or nuclease, or with capsule preventing binding of NETs.
41
Leukocyte rolling
Leukocytes express L-selectin and P-selectin counter ligands (eg sialyl Lewis X). Endothelial cells upregulate presence of P and E selectin in presence of chemokines. Rolling as weak interactions are made and broken,
42
Leukocyte activation
Leukocyte GPCRs rapidly activated by interaction with chemokines, leading change in conformation of cell surface integrins. Integrins can bind tightly to CAM on endothelium = halts rolling and adheres tightly. Beta 2 integrins absent = no effective proceeding from rolling to tight adhesion = Leukocyte adhesion deficiency.
43
Diapedesis
Process of cross endothelial cell layer and underlying basement membrane. Homophilic interaction between CD31 on leukocyte and endothelium as squeezes through gap between cells. Then must cross basement membrane via production of neutrophil elastase. Hence site of inflammation = damaged basement membrane.
44
Necrosis process
Rupture of lysosomes and autolysis Increased density and sequence of morphological changes due to enzymatic hydrolysis of cell components and protein denaturation - Loss of nucleus and clumping of chromatin. Releases DAMPs so stimulating an inflammatory response.
45
Intrinsic pathway of apoptosis
Developmentally programmed and due to response of lack of specific growth factor. Cytochrome C release triggers intracellular caspase release so causing cell death.
46
Extrinsi pathway of apoptosis
External signals act as death receptor which then stimulate caspases. Eg TNf alpha, which has Fas ligand binding to cell surface Fas. Causes a conformational change in Fas such that it binds the death domain - containing adaptor proteins. Adaptor proteins recruit and activate caspase 8, which cleaves caspase 3. Caspase 3 releases the inhibition to CAD which is released to enter the nucleus to cleave DNA. DNA is fragmented into nucleosomal units.
47
Caspase actions
Initiates many proteolytic cascades within the cell. DNA is fragmented into nucleosomal units, and cleaves key enzymes involved in DNA repair and replication, eg: PARPs = DNA repair enzyme DNA topoisomerase II Lamins = intranuclear proteins which maintain nucleus shape.
48
Integration of apoptosis
Following TNF or Fas signalling, the cell is still not fully committed to apoptosis until it receives a further signal to the death domains, or from the BCL family. BCL involved in changing mitochondrial permeability.
49
Mechanism of NETosis
Microbial cues and endogenous activating ROS. ROS activates myeloperoxidase, neutophil elastase and PAD4 to promote chromatin decondensation. NETosis can be either non-lytic (rapid release from lice cells ) or lytic where cell must be disassembled and plasma membrane rupture.
50
Structure of MHC class I
Alpha chain of 45kDa folded into three distinct domain. One end is membrane portion folded into a groove which can accomodate peptides between 7-9 amino acids in length. Polymorphism is mainly localised to the peptide binding groove, and mHC molecules differ in number, orientation and hydrophobil pockets within the peptide binding groove. HLA groups define binding point?
51
MHC class I expression
On all nucleated cells following assembly in the endoplasmic reticulum
52
MHC class II structure
Made of two integral membrane proteins, an alpha and a beta chain, with extracellular bindingg groove for peptide, similar to class I. No disulphide bonds at either end so nothinfg to contrrain the length of peptides to bind.
53
MHC class II distribution
Bind to an extracellular pathogen so onlt present on antigen present cells, in case of possibiity of virus infection.
54
Endogenous pathway of antigen processing and presentation.
``` MHC class I constitutively samples the intracellular environment of the cell. Normal pathway for degradation of misfolded or denatured proteins in order to generate peptides from obligate intracllular pathogens. Proteolsis carried out by the proteasome. ```
55
Exogenous pathway
Macrophagees and dendritic cells can phagocytose pathogens, proteins then delivered to the phagolysosome. Low pH means proteins are rapidly digested to small peptide. MHC class II then transported too endosome to bind peptide components and be presented at the surface of the cell.

AAPathology (9 decks)

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