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Immunology - exam 3 > Dysregulation & Deficiency > Flashcards

Dysregulation & Deficiency Flashcards

1
Q

Ways immune system can dysfunction

A
  • Normal immune response causing pathologic conditions
  • Defects in immune regulation
  • Autoimmune disease
  • Immunodeficiency
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2
Q

People affected by Tuberculosis (TB)

A
  • 1/3 of world is infected panel brick walls
  • Only 5-10% has lifetime risk of developing active TB
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3
Q

Tuberculosis (TB) causative agent

A
  • Caused by Mycobacterium tuberculosis
  • Usually airborne inhaled
  • Pathology created due to normal immune system function
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4
Q

How TB infects person

A
  1. TB modifies surface of phagosome, so it unable to fuse with lysosome within Marcophage.
  2. Therefore TB can thrive/multiples in macrophage
  3. Eventually TB burst out of macrophage, and contents of lysosomes are released into lungs
  4. Inflammatory response is initiated
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5
Q

Results of TB infection

A
  • Person dies, and eventually TB dies too
  • Person recovers: cytokines like INFγ hyperactivates macrophages, which eliminate TB
  • Person lives with chronic infection
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6
Q

Sepsis

A
  • Chemicals are released into the bloodstream to fight infection
  • Inflammation tirggers a cascade that can damage multiple organs –> organ failure
  • Septic shock occurs, blood pressure drops, PT dies
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7
Q

People at risk of Sepsis

A

MC in elderly people

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8
Q

Sepsis Tx

A

IV fluids and antibiotics

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9
Q

Major cytokine involved in Sepsis

A

Tumor necrosis factor (TNF)

  • Increase blood vessel permeability
  • Increase fluid loss
  • Decrease blood pressure and volume
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10
Q

Septic shock

A

Results when positive feedback loops cause overreaction to a system wide infection

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11
Q

Chiropractic Tx for Sepsis

A

Vagal stimulation can decrease macrophage releasing TNF

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12
Q

People affected by Allergies

A
  • 54% of US Pop suffers type I hypersensitivity rxns (MC allergies)
  • Incidence still rising
  • Allergic people respond diff to allergens, than non-allergic people
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13
Q

Allergic vs Non-allergic

A

Allergic

  • STRONG response to allergens
  • Produce much IgE
  • Th2 bias

Non allergic

  • Weak response to allergens
  • Mainly produce IgG
  • Th1 bias
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14
Q

Cells associated with Allergies

A

Th2 bias

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15
Q

Phase one of Allergies

A
  1. FC end of IgE binds to mast cell
  2. Fab end binds to allergen, which triggers mast cell degrandulation
  3. On subsequent exposure allergen can cross link IgE. Cluster sends signal downstream promoting degranulation of mast cell, which release Histamine, Protease, heparin and other chemicals
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16
Q

Phase two of Allergies

A

Immediate = degradulation of mast cells & basophil

  • Mast cells basophils bind IgE
  • Resulting crosslinking of Fc region –> degradulation
  • Cells secrete cytokines (IL-5) which recruit eosinophils

Delayed (chronic) = prominently Eosinophils

• Delayed b/c they must be recruited from bone marrow

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17
Q

Function of mast cells, basophils & eosinophils

A

provide defense against PARASTIC infections (too large for macrophage/neutrophils to phagocytize)

• IgE “guides” mast, baso, eosino to target

18
Q

Why developing fetuses have Th2 bias

A

TH1 releases cytokines (TNF, IL-2) that may consider parental genes as foreign invaders. Thus placenta produces IL-4 which causes both maternal and fetal Th2 bias

19
Q

Heredity and allergies

A

specific gene taken for allergies susceptibility have been identified.

  • Allergy concordance in identical twins is 50%.
  • They may have a new form of IgE receptor that sends high level of IL-4 (promotes class switching of B cells to produce IgE).
20
Q

Glucocorticoids (cortisol)

A

treatment for allergies that works by Th cell production of cytokines thereby activating fewer T cells

  • blocking binding of IgE to mass cells = Xolair
  • histamine blockers = Claritin, Allegra • chiropractic in homeopathy
21
Q

Specific immunotherapy to cure allergies

A
  • injection of gradually increasing doses of crude allergens
  • after several years of regular treatment, patient becomes tolerant to allergen
  • causes the cells to class which from IgE to another class (like IgG)
22
Q

Autoimmune disease

A

results when there is a breakdown in mechanisms meant to preserve tolerance of self

  • affects ~5% of Pop
  • 100 known types
  • incidence is rising,
23
Q

Autoimmune disease causation

A

true reason is unknown

• autoimmune disease Is an unsuccessful adaptation, THOUGHT caused by drastically changing environment in recent history

24
Q

molecular mimicry

A

A hypothesis as to why infection may lead to breakdown of self-tolerance yielding autoimmune disease: Non-self molecule are similar enough to self, thereby causing immune system to activate against self.

25
Q

Molecular mimicry mechanism

A
  1. BCR and TCR have variable affinity which allows them cross react with several antigens with some similarity
  2. During infection, lymphocytes recognize their Cognate antigen associated with microbe.
  3. After infection enough similarity exists between Cognate antigen and Self antigen to cause an AUTO immune response
  4. inflammation must occur in the same tissue that expresses self antigen, in order to activate APCs to re-stimulated self reactive T cells
  5. cytokines generated by inflammation can upregulate MHC I expression on normal cells, thereby making them targets for self reactive CTLs
26
Q

The inflammatory reflex

A

A cholinergic anti-inflammatory pathway that is down regulated by the vagus nerve

27
Q

How molecular mimicry can cause autoimmune disease

A

lymphocytes have receptor that recognize their cognate antigen on a microbe.

  • Receptor recognize a group of antigens, with affinities ranging from high to low (cross reactivity)
  • receptor may cross react with self antigen causing autoimmune disease
  • doesn’t occur prior to infection because affinity is too low, or never brought into contact
28
Q

Re-stimulation of autoimmune T cells

A

When self reactive T cells activated by microbial mimicry reach tissues where they can cross react with self antigens, they must be continually re-stimulated by APCs.

  • It’s not continually restimulated they die via apoptosis
  • if they do not achieve the necessary costimulation, they die via anergized
  • Activation of APCs is triggered by inflammatory cytokines (TNF and IFN-γ) Which is controlled by Innate immune system (Vagus Nerve cholergenic antiseptic reflex)… Inflammation must be in place otherwise T cell would never get co-stimulation necessary to activate
  • Once activated APCs express MHC and co-stimulation molecules necessary for T cell re-stimulated.
29
Q

Myasthenia gravis

A

self reactive antibodies against the Ach receptor prevents Ach from binding, producing muscle weakness and autoimmune dysfunction

• example of autoimmune disease

30
Q

multiple sclerosis

A

immune system attack on myelin in CNS thought to be due to self reactive T cells

• Example of autoimmune disease

31
Q

Rheumatoid arthritis

A

T cells attack cartilage protein in joints. IgM-IgG antibody complexes can activate macrophages leading to chronic inflammation

• example of autoimmune disease

32
Q

Lupus erythemaosis

A

A breakdown between B and T cell tolerance that may affect skin, joints, kidney, brain, and other organs leading to chronic inflammation.

• Example of autoimmune disease

33
Q

Guillian-Barre

A

immune system attack on myeline in PNS

• example of autoimmune disease

34
Q

transverse myelitis

A

An inflammatory process of the spinal cord, and can cause axon demyelination

• example of autoimmune disease

35
Q

Autoimmune Lymphoproliferative Syndrome

A

genetic defect were T cells refuse to die when chronically stimulated by self antigen, due to genetic defect in Fas or Fas Ligand proteins

• example of autoimmune disease

36
Q

criteria for autoimmune disease

A
  • Pt must have MHC molecules that present itself antigen
  • Pt must have T and/or B lymphocyte receptors that recognize self antigen
  • must be environmental factors that breakdown tolerance mechanisms
37
Q

susceptible times for autoimmune disease development

A
  • frequently follows bacterial/viral infection
  • environmental factors
  • chronic inflammation
38
Q

causes of immunodeficiency

A
  • genetic defects: single gene mutations, severe immunodeficiency syndrome (SCIDS)
  • AIDS
39
Q

acquired immunodeficiency syndrome (AIDS)

A

the major cause of human immunodeficiency virus 1 (HIV-1)

  • incidence = 34,000,000
  • Knocks out immune function by targeting T Helper cells • mortality typically due to opportunistic infection
40
Q

HIV infection

A

thought that virus gains access via rectal or vaginal mucosa and infects T Helper cells

  • hijacked cellular machinery to make copies of self and infect other cells
  • chronic phase can last for 10 years or more
  • during chronic phase total number of T helper cells gradually decrease and cripple immune system
41
Q

cells infected by HIV-1

A
  • T helper cells
  • macrophages
  • dendritic cells
  • HIV docs to CD4 protein via GP 120 on Virus
42
Q

treatment for HIV

A

Highly Active Anti-– Retroviral Treatment (HAART)

Immunology - exam 3 (5 decks)

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