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Microbiology > Immune System & Autoimmunity > Flashcards

Immune System & Autoimmunity Flashcards

1
Q

Innate vs Adaptive Immunity

A

Innate - fast response, nonspecific resistance, recognize PAMPs through TLRs, and foreign substances

Adaptive - slow but long lasting, specific resistance - forms antibodies, triggered by cytokines. T and B cells

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2
Q

What are macrophages called in different parts of the body?

A

Alveolar (lungs)
Kupffler cells (liver)
Microglial cells (brain)
Osteoclasts (bone)
Histiocytes (connective tissue)

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3
Q

Function of macrophages

A

Engulf pathogens

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4
Q

Function of NK cells

A
  • Recognize abnormal cells due to decreased MHC-I molecule (or other molecule that normal cells have) as a “non self”
  • Release perforins and granzymes to kill the cell
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5
Q

What do leukocytes start off as?

A

Hematopoietic stem cells in the yolk sac and bone marrow of fetus

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6
Q

Myeloid progenitors become:

A

RBCs
Platelets
WBCs (neutro, baso/mast cells, eosino, monocytes/macrophages, eosino, dendritic cells)

Develop in bone marrow

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7
Q

Lymphoid progenitors become:

A

Lymphocytes (T and B cells, NK cells)

Thymus and bone marrow (for B and NK)

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8
Q

Neutrophil function

A

Phagocytosis

Also has enzymes and microbial properties like lactoferrin (steals iron from pathogens)

First cells to inflammation site

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9
Q

Basophils (in fluids)
Mast cells (in tissue)

Function

A

Allergic reactions and parasites

Granules contain histamine & heparin

Histamine dilates blood vessels so there’s redness at allergic reaction site

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10
Q

Eosinophil function

A

Has toxic compounds that damage parasite cell membrane

Some phagocytic activity

Neutralizes mast cell products

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11
Q

What are the granulocytes?

A

Neutrophils
Basophils
Eosinophils

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12
Q

Agranulocytes

A

Monocytes
Lymphocytes

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13
Q

Monocyte function

A

Matures into macrophages

Phagocytic

Antigen presenting cell to lymphocytes

Produces pro inflammatory cytokines, which attract neutrophils to infection site —> activates NK and T cell differentiation and increases vasodilation to bring more cells and blood to flow

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14
Q

Dendritic cell function

A

Phagocytes

Langerhan cells: specialized dendritic cells that are the most effective APCs (class II MHC - present to T helper cells)

Activate T cells

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15
Q

CR1 (CD35) present on:
(CR1 is the receptor for C3b (which is attached to bacteria))

A
  • RBCs
  • WBCs (Neutrophils, Monocytes/Macrophages, Eosinophils, B & T cells)
  • Follicular dendritic cells

Basically any phagocytic cell

C3b surrounds bacteria and attaches to CR1, then phagocytizes the bacteria

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16
Q

Which cells have TLRs?

A
  • Endothelial cells
  • Dendritic cells
  • Plasmacytoid dendritic cells
  • NK cells
  • WBCs (neutrophils, macrophages, B and T cells)
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17
Q

TLRs function

A

Detect PAMPs on pathogens

First responder to infection

Translocation of transcription factors, cytokine modulation, interferon-stimulated gene regulation (for inflammatory response or antimicrobial release)

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18
Q

Interferon

A

Works against viruses

Protein cytokines trigger:
- Macrophage activation (gamma IFN)
- substances that interfere with RNA viral reproduction (alpha and beta IFN)

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19
Q

Which cells help with worm infections?

A

Eosinophils (parasites)

IgE (worm infection) associated with mast cells & basophils

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20
Q

Cells that help with phagocytosis

A

Macrophages/monocytes

Neutrophils

Dendritic cells

Eosinophils have some phagocytic activity

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21
Q

Complement pathways and their convertase

A
  • Classical pathway: C4bC2a Classical C3 convertase
  • Alternative pathway: C3bBb convertase
  • Lectin pathway: C4bC2a Classical C3 convertase
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22
Q

Classical Pathway (3rd to act)

A
  • C1 binds to IgM
  • C1 + IgM act on C2 and C4 complement proteins
  • this cleaves to C4b and C2a, which helps to cleave C3 —> C3a and C3b
  • C3a: causes inflammation
  • C3b: tags the pathogen for CR1 phagocytosis or C5-9 lysis of pathogen
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23
Q

Alternative pathway

A

Factor B and D and Properdin (helps stabilize convertase) - unique to this pathway

LPS is most potent

Slower than classical

C3bBb convertase

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24
Q

Lectin pathway (2nd to act)

A

Mannose-binding lectin (MBL - acts similarly to C1 protein on Classical pathway) binds with mannose-containing polysaccharides (mannans) on pathogen surface

Similar to Classical pathway, cleaves C4 and C2 to form C4bC2a convertase to cleave C3

25
Q

A and B components of the complement pathways

A

A (float away) - C3a, C4a, C5a - create inflammAtion

C5a - most potent chemotactic and anaphylactic factor

B (binding) - C3b, C4b - tag pathogens - phagocytosis or lysis of pathogens

26
Q

What 2 antibody receptors are present on B cells?

27
Q

Acute immunity status
Primary antibody response

28
Q

Resolving infection
Secondary antibody response

29
Q

Type I Hypersensitivity (mechanism and diseases)

A

Allergic reaction

Antigen on B cell products IgE antibodies, which bind to Fc receptor on mast cell or basophil. During second exposure, the same or similar antigen binds to IgE and the Fc receptors come together and release histamines. Vessels dilate and cause inflammation

Anaphylaxis, rhinitis, food allergies, asthma

30
Q

Type II Hypersensitivity (mechanism and diseases)

A

IgG or IgM bind to surface of normal cells and mark it for destruction using the complement system or Tc

Transfusion reactions, HDN, AIHA, Goodpasture’s syndrome, Hashimoto’s disease, Grave’s disease, Myasthenia Gravis

31
Q

Goodpasture’s Syndrome

A

Lungs and kidneys attacked by collagen antibodies

32
Q

Hashimoto’s thyroiditis

A

Hypothyroidism

33
Q

Grave’s Disease

A

Hyperthyroidism

34
Q

Autoimmune hemolytic anemia

A

RBCs destroyed

Warm (37C) - IgG - spherocytes
Cold (<30C) - IgM - RBCs agglutinate

Jaundice, dark urine, pallor, rapid heartbeat

35
Q

Myasthenia Gravis

A

Neuromuscular disease

Antibodies bind so neurotransmitters cannot attach to stimulate the nerve

Weakness, fatigue, dropping eyelids, cannot speak, chew or swallow

Hypersensitivity II

36
Q

Type III Hypersensitivity (mechanism and diseases)

A

IgG or IgM bind to soluble antigens to form antigen-antibody complex to activate complement, which causes inflammation, vasodilation and attracts neutrophils and macrophages

  • Rheumatoid arthritis, SLE, Arthus reaction, serum sickness
37
Q

Rheumatoid Arthritis

A

Test: Anti-CCP EIA

Systemic inflammatory disease of the joints

IgM binds to Fc receptor on IgG to activate complement

38
Q

Systemic Lupus Erythematosus

A

Anti-smith antibodies

Affects many organs, chronic non-infectious inflammatory disease

39
Q

Type IV Hypersensitivity (mechanism and diseases)

A

Th cells release cytokines to recruit macrophages and neutrophils —> inflammatory response

Tc —> tissue destruction

Delayed response

  • Contact dermatitis, poison ivy, tb test reaction, Celiac disease, Multiple Sclerosis, Type I diabetes
40
Q

Celiac Disease

A

Damages the lining of the small intestine, intestinal villi —> decreased nutrient absorption

Tests: tTGA (antitissue transglutaminase antibody test) and EMA (anti-endomysium abs)

41
Q

Multiple Sclerosis

A

Damage to myelin sheath from self-reactive T cells, crosses blood brain barrier

Tests: oligoclonal bands in CSF

42
Q

Type I diabetes

A

Destruction of Islets of Langerhans cells of the pancreas —> increased insulin production

Tests: GAD (glutamic acid decarboxylase)

43
Q

Polymyositis

A

Inflammation of skeletal muscles and skin

Muscle weakness

Tests: ANA - PM-1 and Jo-1

44
Q

Systemic Sclerosis

A

Hardening/thickening of skin and/or connective tissue

45
Q

Sjogren’s Syndrome

A

Inflammation of salivary and lacrimal glands

Decreased tear and saliva secretion

Anti-SS-A and Anti-SS-B

46
Q

Addison’s Disease

A

Renal deficiency/hypocortisolism

Damage to adrenal cortex - decreased cortisol and aldosterone

Bronze coloration

47
Q

Anti-ds-DNA

A

SLE

homogenous

48
Q

Anti-Sm

A

SLE

Speckled

49
Q

Anti-SS-A (Ro)

A

SLE, Sjögren’s syndrome

Fine speckled

50
Q

Anti-SS-B (La)

A

SLE, Sjögren’s syndrome

Fine speckled

51
Q

Anti-Sci-70

A

Systemic sclerosis, scleroderma

Atypical speckled

52
Q

Anti-Jo-1

A

Polymyositis

Fine cytoplasmic speckling

53
Q

Haptens

A

Nonimmunogenic materials that must be combined with a carrier to illicit an immune response

Ex: poison ivy oil is harmless on its own + skin protein is harmless on its own, but when combined, it’s dangerous

54
Q

What is viral inhibition?

A

Antibodies surround the virus so the virus cannot attach to cells

55
Q

What is neutralization?

A

Antibody called antitoxin binds to the toxin to neutralize it and prevent toxin attachment to cells

56
Q

What is opsonization?

A

Antibodies called opsonins coat the bacterial wall to prevent bacteria from attaching to cells

57
Q

What is Precipitation?

A

Small antigens and antibodies form an arrangement and precipitate out of solution

58
Q

What is Agglutination?

A

Antibodies and antigens on cell surface agglutinate to restrict bacteria’s movement

Microbiology (9 decks)

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