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MIMM 314 > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

what are the primary lymphoid organs

A

-bone marrow
-thymus

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2
Q

what are the secondary lymphoid organs

A

-lymph nodes
-spleen
-peyers patches

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3
Q

what are the 3 signals for activation and differentiation

A

Activation: when it sees its antigen and starts proliferating
Signal 1: present antigen with MHC
Signal 2: co-stimutary molecules ex: cd28 in T cells and B7 in dendritic cells
Differentiation: starts to produce cytokines for T cell. When you start doing stuff
Signal 3: polarizing cytokines. Polarizing: specializes t cells one way or another.
You are polarizing cells to induce gene expression patters that will induce it and then stimulate certain cytokine production by those cells
If a dendritic cell produces IL-12 that is a TH1 polirizing = will start making INFgamma

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4
Q

Why are the lymph nodes the sites for the activation of T cells?

A

-Gathering places where there are lots of opportunity for everyone to show what they are presenting. It is packed with B and T cells and dendritic cells
-They are everywhere in the body, it is close to all barrier tissues. They are at strategic barrier sites like mouth, feet, gut, brain

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5
Q

how do non lymphoid orgrans communicate with lymphoid organs

A

through non resident cells like dendritic cells

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6
Q

what are tissue resident cells vs non resident

A

-Tissue resident immune cells: dendritic cells(these can move and neutrophils too), macrophages and neutrophils that are not circulating through the blood/lymph nodes. It is auto-replenishing within the tissue, they don’t really need to be activated
-non resident they travel all throughout the body

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7
Q

how do leukocytes travel

A

Extensive lymphatic system is the reason why these cells can migrate to the lymph nodes and the tissues and enter the blood circulation

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8
Q

Tissues residents vs circulating leukocytes: what do we need both?

A

-Tissue residents are super fast responders and they are able to sense incoming assaults and communicate with dendritic cells;
-Tissue residents are also very important for the recruitment of other cells and to recognize the antigens and sometimes they don’t even need to to see the antigen to become activated in response to damage signals.
-Because tissue residents are secreting these cytokines to recruit othe cells

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9
Q

true or false: we have more traveling immune cells than resident cells

A

false:
We have more more resident cells than traveling to provide early source of protection

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10
Q

true or false: neutrophils are resident cells

A

false there are evidence that they are able to traverse the non lymphoid barrier

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11
Q

what did Ilya Mehcnikov do?

A

-He was the first to demonstrate phagocytosis and the usefulness of inflammation
-He was studying translucent starfish larvae and stuck a mango thorn in it
-He saw all these cells wrapping all around the mango thorn inside the larvae: these cells are not responsible for causing disease: they protect
-He saw that inflammation was responsible to contain the infection: host defense properties

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12
Q

Neutrophils swarm was then showed 100 years later with the leishmania mouse that was taken to a microscope directly after the infection what can we see with the neutrophils

A

-These neutrophils will swarm at the infected tissues: initial inflammatory step to kill these parasites
-The macrophage come in and eat the neutrophils to stop the inflammation

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13
Q

Why are phagocytes are attacking the infection?

A

-To identify self and non-self to decide whether attack
-If they recognize non self they will attackkkk

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14
Q

what is janeway’s litte secret?

A

-Janeways little secret: adjuvants
-He therorized that innate immune cells must recognize components that are shared across various types of microbes: bacteria, viruses, fungi. Self vs non-self

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15
Q

Ilya was the father of

A

innate immunity

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16
Q

Janeway’s receptors

A

-He called the receptors on macrophages, neutrophils and dendritic cells pattern recognition receptors: PRR ex: Toll like receptors: recognizes some pamps, nods: to recognize bacterial species and the microbial components pathogen associated molecular patterns : PAMPS ex: LPS expressed by gram - bacteria. To recognize gram + lipoteichoic acid
-This treaty also applies how adjuvants work: they contain some pamps that cells recognize through PRRs

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17
Q

What is a TOLL discovery?

A

-The development of the fruit flies uses this toll pathway to grow: used in adulthood for protection against pathogens: the TOLL receptors
-This also applies to humans: janeway proved that we have TOL like receptors too
-The start of how the immune system senses pathogens

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18
Q

What is a limitation of Janeway hypotheses?

A

the mango thorn is not a pathogen

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19
Q

Matzinger’s danger theory

A

Pamp theory is not enough
She theorized that innate immune cells not only recognize microbial patterns but also sense other forms of danger including indicators or cell stress/dysfunction/death

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20
Q

damps def

A

Coined the term danger associated patterns : DAMPS: include both microbial and non-microbial inflammatory triggers
danger associated molecular pattersn

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21
Q

Sterile inflammation def and ex

A

-Sterile inflammation:when you have tissue damage in the absence of any microbial agents and the absence of overt infection
-Sterile inflammatory events: obesity because damage response without any microbials, bruising: tissue damage

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22
Q

true or false: if you cut your skin, that is a sterile inflammation event

A

If you have microbes on your skin= that means that it is not sterile

23
Q

Neutrophils also go to sites that are burned like the liver with a laser. what does it show?

A

This is an example that her danger theory works because it is a sterile inflammatory events

24
Q

true or false: neutrophils can respond to different things

A

true
Neutrophils can respond to different things which means that they are likely to do different things

25
Q

Inducers of inflammation

A

-Exogenous:
_Microbial ex: pamps, ex: pathogen RNA, DNA, cell membrane components and virulence factors ex: bacterial toxins
_non-microbial : allergens, irritants, foreign bodies, toxic compounds like the mango thorn

-Endogenous: signals released from stressed, malfunctioning or dead cells and from damaged tissues. Endogenous crystals. Products of ECM breakdown. Some are called alarmins which are produced by cells and dying cells
_Cell derived
_Tissue derived
_Plasma derived
ECM derived

26
Q

Core components of inflammation

A

Inducers (stimulants) -> sensors (sense inducers: detectors like PRRs) -> effectors (cell types ex: neutrophils could be lymphoid or non lymphoid) -> mediators (soluble factors ex: cytokines, chemokines (recruitment factors to call backup), antibodies, antimicrobial peptides

27
Q

ex of cytokines

A

Cytokies: interleukin 1, thf-a, IL-33

28
Q

ex of chemokines

A

Chemokines: CXCL1, CCl2

29
Q

ex of antimicrobial peptides

A

Antimicrobial peptides: RegIIIy

30
Q

ex of antibodies

A

IgE

31
Q

ex of lipid mediators

A

Lipid mediators: leukotrienes, prostaglandins

32
Q

is obesity a sterile inflammatory event

A

is a sterile event because the adipocytes expand and puts tissue stress on the organs and leads to inflammation. It is a chronic inflammatory event

33
Q

Inflammatory response can be too much of a good thing=

A

Inflammatory response can be too much of a good thing= immunopathalogy

34
Q

true or false: the system is made to handle the damage from the immune system

A

false:
-The system is not set up in a way that prevents the damage from the immune system. There is no way for the system to only kill virally infected cells ex: the flu when we get sick, we get sick because of our immune response that is not shut down. The immune response makes you sick, hence why we need to shut it off.
-When people go to the hospital because of covid it is usually because they were not able to modulate the immune response
-We need to be able to modulate the immune response

35
Q

could too much inflammation lead to chronic inflammation

A

true
Too much of inflammation = chronic inflammation which could put you more at risk of other inflammatory events. Obesity can lead to that

36
Q

Inducers and mediators are required to maintain….

A

-Inducers and mediators are required to maintain homeostasis aka a return to normal: we are working towards some type of harmony
_Control of homeostasis and disharmony
_We are always in a state of disharmony, we’re eating junk food, get sick etc, we want to work towards the harmony
_We are always in a certain state of inflammation

37
Q

how do we define the balance of the homeostasis

A

the structure of the tissues

38
Q

The location of cells and how their ability to interact in a physical way will determine

A

The location of cells and how their ability to interact in a physical way will determine the degree of inflammation that we experience

39
Q

Physiological inflammation:

A

Physiological inflammation: below the radar: the top cells are constantly sensing stuff. On going low inflammatory response

40
Q

overt , protective inflammation

A

-When you have local inflammatory responses like if you have a sterile inflammation in the liver
-Contained at that site, it does not have systemic effects

41
Q

Overt Damaging inflammation

A

Ex: if you have a bacteria that is in the bloodstream, then it will have systemic effects

42
Q

The hierarchy of inflammation

A
  1. Structure (base aka the most important)
    -We need tissues that are structured in a way that have evolved to be protective and allow us to function in a dynamic environment.
    -If this fall apart then we can’t regulate ourselves
  2. Function
    If this changes then there might have some inflammation
  3. Regulation
43
Q

What are 3 factors that may determine the severity of an inflammatory response

A

-Tissue
-Sterile or not sterile
-The infectious dose or the magnitude of injury
-Age, diet, microbiome, if they have an ongoing condition

44
Q

How does matzinger theory differ from Janeway self vs non-self

A

Matzinger incluses self and non self concept but it emcopasses the possibility of the tissues being damaged and inducing a response

45
Q

What is the difference between a circulating and tissue-resident immune system

A

-Resident don’t leave where they are and they are self rewiewing, not replenished by circulating cells ex: macrophages
-Circulating: T cells, dendritic,

46
Q

If we have immune cells resident to ro surveying non-lymphoid organs, Why do we need secondary lymphoid organs

A

-Residents cells are innate and lymphoid organs are there for the adaptive to expand and specify
-There are as a gathering place for naive T cells since they can’t travel in non lymphoid tissues

47
Q

what was the first definition of pain from 1979

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described

48
Q

what is a fact that disproved the first def of pain

A

masochism
-masochist don’t find pain unpleasant

49
Q

what are the reasons why some people are masochists

A

-we find pain pleasant in the irght moments
-some people get their rocks off when there is pain involved

50
Q

examples of non unpleasant pain

A

-spicy food
-tattoos
-exercise
-scratching

51
Q

second oldest def of pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

52
Q

What is wrong with that definition:an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

A

-it assumes that the more rthere is an input the more it is gonna hurt, but sometimes the damage is into the nerves and it hurts really bad, more than a punch which is false
-it does not account for perceptual change since at some point if you have excruciating pain it will hurt less
-the pain does not equal the state of someone, the level of pain depends on the person

53
Q

true or false: the more time you are in pain the less you will feel it

A

false; you will feel it more

MIMM 314 (11 decks)

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