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PSY333 > Psychoneuroimmunology > Flashcards

Psychoneuroimmunology Flashcards

1
Q

What is PNI?

A

The study of the effect of the brain on health and resistance to disease (the immune system).
Study of interactions between CNS and immune
system.

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2
Q

Immune system can be…

A

conditioned

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3
Q

The mind can…

A

effect the ability to fight disease

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4
Q

What are the key pathways in the old model of the stress response (HPA axis)?

A

Hypothalamus → CRH → Pituitary → ACTH → Adrenal Cortex → Cortisol → Affects immunity

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4
Q

What are the key pathways in the old model of the stress response (SAM axis)?

A

Locus coeruleus → Sympathetic Nervous System → Adrenal Medulla → Catecholamines → Affects immunity

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4
Q

The old model is…

A

top-down & says CNS drives immune system

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4
Q

What is the goal of the immune system?

A

to defend against pathogens

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4
Q

How do the nervous, endocrine, and immune systems interact in the new PNI model?

A

Stressor affects Nervous, Endocrine, and Immune systems.

Nervous system ↔ communicates via neurotransmitters & cytokines.

Endocrine system ↔ communicates via hormones & neurotransmitters.

Immune system ↔ communicates via cytokines & hormones.

All systems interact bidirectionally.

Linked to conditions like anxiety, depression, insomnia, inflammation, infections, allergies, and pain.

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5
Q

How does the immune system work

A

locates pathogens and activates processes to eliminate them

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5
Q

Why is the immune system important

A

Protects from disease but is also a mechanism by which stress can cause disease

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5
Q

What pathogens do we need protection from?

A

Prokaryote (bacteria) & Virus (HIV)

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6
Q

Non-specific immune mechanism

A

general set of responses to any kind of invasion (built in)

prevents pathogens from getting in and kills them if/ when they do

operates the same whether or not your body has seen the pathogen before

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6
Q

Specific immune mechanism

A

learned immunity based on past experience (exposure, vaccines)

protects against specific pathogens and their toxins

utilizes anti-bodies to target specific pathogens via antigens

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7
Q

2nd line of non-specific immunity

A

innate immunen cells > inflammatory response

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7
Q

2nd line: chemical way

A

Haematopoiesis (mother cell) > Commom lymphoid progenitor

macrophage: eater cell, important to deal with pathogens

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7
Q

1st line of non-specific (physical barriers)

A

Skin (prevents entry) > mucous membrane (traps dirt) > gut bacteria (out compete bad)

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8
Q

Second line: inflammatory response

A

Mast cells: produce histamine which leads to inflammation and draws more lymphocytes (white blood cells) to the area

causes inflammation, swollen lymph nodes, fever, local swelling

goal of inflammation is to kill invader and restore damaged tissues

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8
Q

3rd line Adaptive/ acquired immunity

A

specialised lymphocytes (when things get serious)
1. humoral immunity
2. cell-mediated immunity (macrophage> T helper> B cells> antibodies) (macrophage> T helper> T cells> cytotoxic killer cells)

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9
Q

What do anti-bodies do

A

(is specific to the antigen) & attaches to and tags invading cells so phagocytes can find and eat them

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9
Q

Macrophages

A

second line innate immune cell

…is a type of phagocyte that ingests the pathogen and releases cytokines to signal to other immune cells that there is an intruder

also natural killer cells, neutrophils

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10
Q

Humoral immunity (antibody mediated immunity)

A

acts before cells get infected

protect against bacterial and viral reinfection

B-cells produce and secrete anti-bodies that recognise specific antigens (proteins on the surface of bacteria and viruses that the body recognises as foreign)

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11
Q

Cell-mediated immunity

A

after cells are infected

slower acting

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12
Q

T cells

A

release chemicals that target and destroy infected cells

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13
Q

Tc

A

Cytotoxin: toxin to cells- respond to specific antigen

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14
Th
helper: of process
15
Tcm
memory cells
16
What is the first step in acquired immunity?
An antigen-presenting cell (APC) presents a foreign antigen on its MHC (mature helper cell), which is recognized by an immature T-cell via its T-cell receptor (TCR)
17
How do T cells respond after encountering an antigen presented by an APC?
T cells differentiate into: CD8+ Cytotoxic T cells, which destroy infected cells. CD4+ Helper T cells (Th cells), which coordinate immune responses by releasing cytokines.
18
What do cytotoxic T cells do in the immune response?
They destroy cells infected by the pathogen.
19
What do helper T cells (Th cells) do?
They secrete cytokines to: Activate B cells Enhance the bactericidal activity of macrophages
20
What triggers B cell activation?
A B cell receptor binds to a matching antigen, which is ingested and presented. Then, helper T cells interact with the B cell and secrete cytokines to activate it
21
What do activated B cells become?
They multiply and differentiate into: Plasma cells (which produce antibodies) Memory B cells (which remain for faster future responses)
22
What is the function of plasma cells?
Plasma cells produce antibodies that: Bind to matching antigens on pathogens Cause neutralization Trigger complement activation Promote phagocytosis by forming antigen-antibody complexes that are eliminated
23
Why are memory B cells important?
They remain in the body and respond rapidly to subsequent infections by the same pathogen.
24
What initiates the immune response in the diagram?
An infectious agent
25
Cytokines
cell communication system, affect immune system, can cross BBB and go to hypothalamus for hormonal response (eg. macrophage, lymphocyte, mast cell, endothelial, fibroblast, granulocyte)
26
Immunogen
specific type of antigen that is able to elicit an immune response (inactivated virus, viral subunit, mRNA vaccines- fastest) type of immunogen impacts what type of immune response is induced
27
A healthy person has...
low/ moderate levels of white blood cells should show an increase in white blood cells in the presence of antigens/ pathogens
28
Immunocompetence
the overall ability of the immune system at any given time to defend the body against the harmful effects of foreign agents
29
immune deficiency/ immunocompromise
inadequate immune response (natural or side effect of drugs) eg. aids an immune deficiency syndrome caused by HIV virus
30
methods for assessing immune system functioning
blood tests for T cell counts, cytokines and other types of white blood cells
31
allergies
oversensitive immune system, misidentifies innocuous substances as harmful, mast cells release histamines rates have been increasing because of pollution and microbial deprivation
32
autoimmune
overactive immune system, body attacks itself ex. rheumatoid arthritis, crohn's disease all characterised by inflammation and treated via anti-inflammatories and immunosuppressant drugs. side effects of this include reduced immunocompetence
33
seyle's general adaptation syndrome
3 stages of bodily response to stress
34
stage 1 of stress: alarm
fight or flight, mobilize energy, release cortisol, EPI and NE
35
stage 2: resistance or adaptation
if stress is involved- return to homeostasis and if not body continues in state of arousal despite depleted energy
36
stage 3: exhaustion
chronic stress leads to burnout, damage to brain and body, memory impairment, anxiety and depression, immune system compromised
37
criticisms of general adaptation syndrome
assumes responses are uniform: - not all stimuli produce same response (car crash vs spilled milk) - not all people respond the same way to the same stressors - does not discuss the role of psych appraisal
38
diathesis stress model
assumes two factors produce disease 1. predisposition to the diseases (biochemical or genetic or smg in childhood) 2. expereince some sort of stress protective factors can mitigate impact of stress
39
stress and immune system: glucocorticoids
shrink thymus gland (where T cells are from), halt informaton of new lymphocytes block release of interleukins and interferons making circulating lymphocytes from circulation kills T lymphocytes
40
stress ST
immune enhancement
41
stress LT
immune supression
42
Chronic stress
- changes HPA axis, - overactive immune system, - excess release of cytokines and inflammation, - cytokines and elevated levels of glucocorticoids associated with depression - disrupt the serotonergic system
43
What is the Sickness Hypothesis of Depression?
It suggests that increased inflammation (via pro-inflammatory cytokines) contributes to the development of depressive symptoms.
44
inflammation affects...
environment, lifestyle, psych factors
45
inflammation: trauma and cardiovasuclar disease
trauma> dysregulated HPA and SAM axis > immune dysregulation> accelerated bio aging > incident CVD
46
What evidence supports the Sickness Hypothesis?
Cytokine treatment increases depression in non-depressed patients Depression often precedes somatic signs in pancreatic cancer and AIDS Antidepressants can reduce inflammation Links autoimmune disease and depression
47
What is the Social Signal Transduction Theory of Depression?
It proposes that chronic interpersonal stress leads to inflammation, which increases risk for depression.
48
What do pro-inflammatory cytokines affect according to this theory?
Sleep, appetite, libido, social behavior, and mood—all core depression symptoms.
49
Is inflammation a correlate or cause of depression in this context?
It's both a correlate and a risk factor, especially under chronic stress.
50
iummunogen: inactivated virus
dead virus advan: induces strong antibody response disad: requires large qunatities & low or no cellular response ex. influenza, rabies, hepatitis A
51
iummunogen: viral subunit
a protein derived from a pathogen advan: may have fewer side effects than whole virus disad: may be poorly immunogenic & complex process ex. influenza
52
iummunogen: viral vector
viral pathogen expressed on a safe virus that doesnt cause disease advan: rapid development, strong cellular response, rel easy to produce disad: prior exposure may reduce immunogenicity, some require boosting ex. ebola
53
iummunogen: nucleic acid
mRNA coding for a viral protein strong cellular immunity & rapid development rel low antibody response & not LT COVID-19
54
What does a traditional vaccine do?
It activates adaptive immune cells, triggering an adaptive immune response.
55
What role do B cells play after vaccination?
They produce antibodies that prevent viruses from entering cells.
56
What role do T cells play after vaccination?
They kill infected cells to stop the virus from replicating.
57
What are the two main arms of the adaptive immune response activated by vaccines?
B cells – produce antibodies (humoral immunity) T cells – destroy infected cells (cell-mediated immunity)

PSY333 (7 decks)

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