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Medical immunology > week 21 p1 > Flashcards

week 21 p1 Flashcards

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USMLE® Step 1 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
Q

what is the function of B2

A
  • 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
Q

What is Natural killer T cells

A

• 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
Q

Where is Natural killer T cells are located

A

NK T cells selected in thymus and found in liver, spleen and bone marrow

28
Q

What is the function of natural T killer cells

A

• 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
Q

What does “Missing-self”: NK cell recognition

A

• Innate Immunity’s cells that recognise and kill virus-infected and abnormal cells

Either inhibit or regulatory NK cells

30
Q

What does Nk cells express an array of receptors

A

• Balance of signals from activating receptors and inhibitory receptors on the NK cell surface.

31
Q

What does NK cells express

A

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
Q

What is apoptosis

A

A programmed chain of events is triggered in the target cell

• kills the ghost cells so this cannot continue to make pathogens

33
Q

What does apoptosis cause

A

• Nuclear “blebbing”

Cell membrane remains intact

Shedding of small membrane vesicles

Apoptotic bodies” removed by phagocytic cells

34
Q

What does it mean by necrosis

A

• If a cell dies by necrosis (i.e. if it “pops”) pathogens will be released

thus propagating the infection

35
Q
  1. What is Inflammation
A
  • An immediate response to damage to its tissues and cells by:
    • Pathogens, chemicals and physical injury
36
Q

How does Acute inflammation

A

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
Q

What is Chronic inflammation

A

• 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
Q

What is the linkage between cancer and inflammation

A
  • 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
Q

what is the complement system

A

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
Q

Interface between innate and adaptive immunity: Complement

A

• 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
Q

How does c3 play a vital role in B cells

A

• 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
Q

What is Interface: Waste disposal

A

• 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
Q

What is the genetic defects Complement system in neuroinflammation and neurodegeneration

A 
• 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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