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Mike's topics Flashcards

1
Q

Inflammation

A

the immune system’s response to harmful stimuli, such as pathogens, damaged cells, toxic compounds, or irradiation

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2
Q

Leukocytes

A

Types of leukocytes are granulocytes (neutrophils, eosinophils, and basophils), monocytes, and lymphocytes (T cells and B cells)

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3
Q

Phagocyte types

A

Neutrophils, macrophages

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4
Q

Surface receptors on neutrophils

A

Fc receptors: CD16, CD32, both binds to IgG -antigen complexes

Complement receptors: C5aR, CD35, CD18

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5
Q

What are monocytes

A

Blood borne precursors of macrophages

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6
Q

Opsonization

A

Process of making a microbe easier to phagocytose

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7
Q

What does opsonins include

A

Complement component C3b and antibody

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8
Q

Surface receptor on NK cells

A

Fc receptors: CD16

Inhibition receptor: KIR
Activation receptor: KAR

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9
Q

Mechanism of NK cells being activated and kill virus infected cell?

A

Infection of cells by some viruses reduces the expression of MHC molecules, thus decreasing the loading of class I peptides in HLA-E, allowing the activation through KARs to induce NK cells killing of the infected cell

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10
Q

Which mediators attract neutrophils and eosinophils

A

TNFa, IL8, IL5

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11
Q

What does dendritic cells do

A

Recognize microbial antigens through innate receptors, and initiate adaptive immune response by presenting peptide antigens to T helper (CD4) cells

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12
Q

Role of eosinophils

A

Mainly responsible for killing large parasites which cannot be phagocytosed

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13
Q

What does phagocytes do

A

Attracted to the site of infection (chemotaxis), bind to the microbe (adhere), ingest (phagocytose), and kill the microbe

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14
Q

What does NK cells do

A

Changes in the surface molecules of cells as the result of virus infection allow NK cells to bind to and kill infected cells by releasing perforins and inducing apoptosis. On binding to virus infected cells, NK cells secrete interferon gamma which protects adjacent cells from being infected

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15
Q

What does mast cells and basophils do

A

When activated, these cells degranulate, releasing a pharmacological mediators which cause vasodilation, increased vascular permeability and leukocyte migration

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16
Q

Type I interferon is induced by…

A

Virus; other cytokines (e.g. IL1, TNFa); intercellular bacteria and protozoans

17
Q

Type I interferon is produced by…

A

Infected leukocytes; epithelial cells, fibroblasts

18
Q

What does type I IFN do

A

Inhibit protein synthesis, mRNA translation, and DNA replication -> stop viral replication; stop cell proliferation; increase the lytic activity of NK cells; induce the expression of MHC class I molecules to induce antigen-specific cytolytic T cell response against viral infected cells

19
Q

What does IL-1, IL-6, TNF-a do

A

Increasing body temp, increase lymphocyte activation, mobilize neutrophils by increasing vascular permeability; induction of acute phase protein release (CRP, MBP) and thus complement and opsonization

20
Q

Which TLRs can recognize virus

A

TLR 243789

21
Q

Which TLR recognize viral RNA

A

TLR 378

22
Q

Cell surface TLRs

A

TLR 1245

23
Q

Endosomal TLRs

A

TLR3789 13

24
Q

Molecular mechanism of TLR4 recognition of LPS?

A

Since the interaction between TLR4 and LPS is relatively weak, it needs the help of effector proteins, namely MD-2, LBP, and CD14.
1. MD2 forms stable interactions with the extra cellular domain of TLR4, forming a functional LPS receptor complex
2. soluble LBP in the plasma bind to LPS and transfer it to either the receptor complex or to CD14
3. CD14 transports LPS-LBP to the receptor complex
4. 5/6 acetyl chains of LPS binds to the hydrophobic pocket of MD2. The rest one attach to TLR4. Two phosphate groups of LPS also bind to both TLR4 and MD2

25
Q

Examples of TLR4 recognizing viral components?

A

Influenza matrix 1 protein
RSV cell surface exposed F protein
HIV tat protein

26
Q

TLR3 is mainly expressed by

A

DC, fibroblasts, intestinal epithelial cells

27
Q

Physiological ligand for TLR3

A

RNA species of West Nile virus, encephalomyelitis virus, Zika virus, dsRNA intermediates of DNA virus such as HSV-1

28
Q

PRR

A

pattern recognition receptor, innate immune receptor that recognizes PAMPs/MAMPs and induces PAMP-trigged immunity

29
Q

PAMP

A

pathogen-associated molecular pattern, immunogenic conserved molecular motif shared across many pathogens and absent from the host, also referred to as MAMP (microbe associated molecular pattern)

30
Q

DAMP

A

immunogenic host molecule associated with host tissue damage

31
Q

six overlapping general mechanism of innate sensing

A

PTI, ETI, sensing of absence of self, sensing of altered self, damage recognition, surveillance

32
Q

examples of sensing of absence of self

A

1) NK cells and viral infected cells with decreased MHC I expression
2) CD47 being a self recognition signal, sent to macrophage and dendritic cells

33
Q

examples of sensing of altered self

A

1) cells non-autonomously induce the apoptosis of the virally infected or transformed cells
2) the detection of stressed host cells by NK cells via recognition of MICA and MICB which are induced upon viral infection

34
Q
A
35
Q

What happens upon TLR activation

A

Once activated, TLR undergo a conformational change which leads to recruitment of adaptor proteins to the intracellular signaling domain (TIR). Adaptor proteins include MYD88, TRIF, TIRAP, or TRAM.
Downstream signaling cascade will be activated which eventually leads to the translocation of transcription factors (NF-kB, AP1, IRF3/ITF7) into the cell nucleus, resulting in the expression of key genes of the innate immune system.

36
Q

TLR3 recognize

A

Viral dsRNA
Small interfering RNA
Self-RNA derived from damaged cells

37
Q

TLR7 recognize

A

Predominantly expressed in pDCs
Recognize ssRNA from viruses

38
Q

Defining features of SLE

A

Breakdown of tolerance to nucleic acids
Activation of the interferon system

Comps (5 decks)

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