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Medical immunology > week 21 p1 > Flashcards

week 21 p1 Flashcards

1
Q

What is complement Innate and Adaptive Interactions

A

• Activated by IgM and IgG immune complexes – Classical pathway via C1q fragment
• Drives infection clearance
Drives the Inflammatory response, e.g. in autoimmune disease states

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2
Q

What is the factor in T cell activation by DC

A

• Complement receptors and regulators on DC modulates:
• their maturation status via cytokine and chemokine expression profile
• These immunological ‘hormones’ direct the type of response made by T-cells during the cognate antigen-presenting cell –T cell interaction.
• Timing is critical but……C1q binding / opsonised immune complexes bind T cells via a C1q receptor can lead to T-cell activation
T-cell activation +/- T-cell receptor stimulation -> cytokine release, e.g. gamma-interferon, Tumour Necrosis Factor

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3
Q

What is dendric cells

A

• At the junction of innate and adaptive immunity
• Bone marrow derived.
• Immature cells reside in periphery
through Uptake of antigen in peripheral sites.

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4
Q

What is the role of MHC-II to extracellular antigen

A

• MHC CLASS II is found on the antigen
• Recognised by T helper cells
• Take in antigen in the cell for phagocytosis to happen
Then travels to the cell surface

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5
Q

How does DC is activated by pathogen internalisation and antigen presentation

A

Co stimulatory and adhesion molecules

Cytokine production

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6
Q

how do PARP-PRR get recognised by Microbial pathogen recognition

A
  • Transmembrane PRRs: Toll-like receptors (TLR) and C-type lectins (CTL)
    • Secreted PRRs: collect ins, ficolin’s, pentraxins, and recognition subcomponents of the complement system

Cytosolic PRRs: Retinoic acid-inducible gene I (RIGI)- like receptors (RLRs) and nucleotide-binding domain and leucine-rich repeat-containing receptors (NLRs)

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7
Q

How does the activation of DC happen by pathogens

A
  • Different toll like receptor (TLR) binding results in secretion of different cytokines
    • CD8-/86 expression induced by TLR and delivers

Secondary signals to T cells

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8
Q

What does it mean by tolerance

A

• Normal clearance

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9
Q

What is danger

A

Immunogenic clearance

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10
Q

How does this tolerance and vs danger happen in the immunity

A

• TLR expresses ion by DC forms the basis for activation of the immune cells

As opposed to tolerance if the T cells sees antigen on the cell first

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11
Q

What does it mean by Decoding the patterns of self and non-self

A

Involves recognition of:
○ microbial non-self
○ missing self
induced or altered self

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12
Q

What does it mean by the recognition of microbial non self

A

• Activation of TLRs on professional APCs (DCs) induces expression of co-stimulatory signals for naïve T cells.

PAMP-induced expression of co-stimulators flags antigenic peptides as non-self.

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13
Q

How can Self peptides presented are not recognised because

A

• they are not flagged.

T cell specific for these peptides are clonally deleted in thymus (negative selection)

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14
Q
  1. How can the Regulation of adaptive immune response be by innate immune response
A
  • Most PRRs activate intracellular factors that stimulate DNA transcription, cytokine production and cell survival
    • Secreted PRRs and endocytic PRRs do not induce adaptive immunity themselves

Microbial stimulators of TLRs -> activate inflammation, tissue repair and adaptive immunity.

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15
Q

Why does T cells recognise so many antigens

A
  • Each developing T cell expresses a different receptor; each T cell expresses only one type of T-cell receptor (TCR)
    • diversity is generated by ‘mixing and matching’ genes segments within the four genes that encode TCRs a, b, g, d

So no gene as that woukld require tens of million of different genes

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16
Q

How does antigens receptor diversity occur

A
  • Recombination of TCR genes is random
    • can generate receptors that recognise MHC +

self-reactive T cells must be removed or controlled

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17
Q
  1. How does Specialised lymphocytes bridge the innate and adaptive immune responses
A

• Innate immunity- occurs within hrs

Spelised lymphocytes and adaptive immunity occur in weeks

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18
Q

What is Gamma-delta T cells

A
  • Express antigen receptors of limited functional diversity
    • Provide protection at epithelial and systemic sites until the development of adaptive immunity
    • May have a role in anti-inflammation and tissue repair later in the immune response
19
Q

What is located in T cells of mucosal surface Intraepithelial lymphocytes (IEL)

A

IELs found in bowel supporting epithelial integrity

98% are cytotoxic T-cells and mainly alpha-beta T-cells

20
Q

What is the function of IEL

A

• Do not need priming as antigen-experienced so:
• Kill infected cells
Release cytokines that help with the B-cell responses

21
Q

What can ILEL cause

A

IEL numbers: raised in coeliac disease

Cause Type IV hypersensitivity reactions

22
Q

What is type 1 B cells

A

• Are detected in spleen, intestine, peritoneal cavity

Found in foetal and neonatal development – produced in foetal liver, embryo skewed towards B1-cell development

23
Q

What is the function of B1 cells

A
  • Produce “natural” immunoglobulin M (IgM) and IgA, which is largely encoded by germline immunoglobulin genes.
    • Marginal zone B cells make antibody response to blood-borne infections

Ability to respond to isotype switching, e.g. IL-4, may be secondary to the production of IgM.

24
Q

What is B2 cells

A

Represent the majority of B-lymphocytes secreting immunoglobulins

25
what is the function of B2
* B2 cells are mostly seen as atherogenic,(promote fatty deposits in arteries) while B1 cells as athero-protective * can produce high-affinity antibodies To note: Cardiovascular (CV) events resulting from accelerated atherosclerosis, are an important cause of mortality in patients with Systemic lupus erythematosus (SLE) – a systemic autoimmune disease.
26
What is Natural killer T cells
• Heterogeneous group of T cells that share properties of T cells and Natural Killer cells lymphocytes that express both a T-cell receptor (TCR) alpha-beta T-cell receptor + NK1.1 cell marker
27
Where is Natural killer T cells are located
NK T cells selected in thymus and found in liver, spleen and bone marrow
28
What is the function of natural T killer cells
• Activated NKT cells release cytokines (e.g. IL-4, IFN-gamma, TNF-alpha) • Defend against bacteria undetected by TLRs • Specialised for detection of glycolipid Ag • Enhance antibody-immunity- protect for viruses Dysfunction of NKT cells implicated in autoimmune diseases, some cancers, asthma.
29
What does “Missing-self”: NK cell recognition
• Innate Immunity’s cells that recognise and kill virus-infected and abnormal cells Either inhibit or regulatory NK cells
30
What does Nk cells express an array of receptors
• Balance of signals from activating receptors and inhibitory receptors on the NK cell surface.
31
What does NK cells express
Activating receptors recognise cell surface molecules on cancer cells and infected cells, -> ‘switch on’ the NK cell. Inhibitory receptors recognise the MHC I on surface of cells -> restrain NK cells
32
What is apoptosis
A programmed chain of events is triggered in the target cell | • kills the ghost cells so this cannot continue to make pathogens
33
What does apoptosis cause
• Nuclear “blebbing” Cell membrane remains intact Shedding of small membrane vesicles Apoptotic bodies” removed by phagocytic cells
34
What does it mean by necrosis
• If a cell dies by necrosis (i.e. if it “pops”) pathogens will be released thus propagating the infection
35
34. What is Inflammation
* An immediate response to damage to its tissues and cells by: * Pathogens, chemicals and physical injury
36
How does Acute inflammation
Delivery of plasma and leukocytes to site of injury Recruitment of macrophages & mast cells Production of chemokines, cytokines, vasoactive amines, eicosanoids and products of proteolytic cascades Elimination of stimulus (eg, infectious agents) Resolving and repairing the site of injury
37
What is Chronic inflammation
• Prolonged, dysregulated and maladaptive response that: • Is associated with chronic diseases, e.g. allergy, atherosclerosis, cancer, arthritis and autoimmune diseases • Is found as active persistent inflammation • Is detected with tissue destruction Attempts at tissue repairs
38
What is the linkage between cancer and inflammation
* Inflammatory conditions are present before a malignant change occurs * helps in the proliferation and survival of malignant cells * promotes angiogenesis and metastasis * subverts adaptive immune responses alters responses to hormones and chemotherapeutic agents
39
what is the complement system
complement components circulating in the blood, the lymph, and the interstitial fluid secreted mostly by the liver and encompass the PRR components and the effector molecules
40
Interface between innate and adaptive immunity: Complement
• Augmentation of antibody response: • C3b and C4b bound to immune complexes and to antigens • C3 receptors on B cells and APCs • Enhancement of immunologic memory:C3b and C4b bound to immune complexes and to antigens C3 receptors on follicular dendritic cell
41
How does c3 play a vital role in B cells
• CD21-mediated signals also directly control positive selection and the expansion and maintenance of a subset of B cells termed B-1 cells Furthermore, and aligning with the growing understanding that complement also contributes to the negative control of immune responses and even immune cell homeostasis (1
42
What is Interface: Waste disposal
• Clearance of immune complexes (Ag-Ab complex) from tissues: • C1q covalently bound fragments of C3 and C4 Clearance of apoptotic cells:C1q , Covalently bound fragments of C3 and C4
43
What is the genetic defects Complement system in neuroinflammation and neurodegeneration
``` • Alzheimer’s disease (AD) • Familial dementia (FD) • Parkinson disease (PD) • Guam Parkinson–dementia complex • Huntington’s disease (HD) Prion diseases ```

Medical immunology (5 decks)

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