Organ-specific immunity: LUNG Flashcards

1
Q

What type of branching system does the lungs have?

A

Dichotomous

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2
Q

What does the respiratory unit consist of?

A

The respiratory bronchioles and alveolar ducts

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3
Q

What do the conducting airways consist of?

A

Trachea, segmental bronchi and nonrespiratory bronchioles

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4
Q

What is found in the submucosa of the bronchus?

A

Cartilage and glands

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5
Q

What type of epithelium is that of the bronchus?

A

Pseudostratified

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6
Q

What is BALT?

A

Bronchus-associated lymphoid tissue

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7
Q

Does BALT have germinal centers?

A

Yes

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8
Q

What is the difference between BALT and lymph nodes?

A

LNs are more well defined and have a capsule with afferent and efferent lymphatic vessels for fluid circulation

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9
Q

What are club cells?

A

Clara cells. They are nonciliated bronchiolar secretory cells that secrete surfactants, and are progenitors for other cells

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10
Q

Is the beating of cilia ATP dependent?

A

Yes

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11
Q

What causes ciliary dyskinesia?

A

Disorder of motor proteins within cilia

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12
Q

What causes cystic fibrosis?

A

Mutations that affect chloride ion channels, preventing them from getting to the cell surface, leading to thick sticky buildup and flattening of cilia

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13
Q

What does ciliary dyskinesia lead to?

A

Mucus buildup with dirt and bateria

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13
Q

What influences mucus production?

A

DNA of damaged cells

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14
Q

What is a risk factor for tumorlets?

A

Chronic or repeated inflammation, causing consistent increase in neuroendocrine bundles aka hyperplasia

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14
Q

What is metaplasia?

A

A change of one cellular phenotype to another

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15
Q

What is the CTFR?

A

Ion transporter that regulates mucus viscosity

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16
Q

What does surfactant do?

A

Lower surface tension to be able to breathe more easily

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17
Q

Why is the pleura being so thin important?

A

Negative pressure between the lung and the thorax

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17
Q

Why is pulmonary infection the most common type of infection?

A

Exposure/interface with the environment

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18
Q

What is one problem with histological diagnosis of viral pneumonia?

A

Limited morphological specificity

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18
Q

What is a typical infection dynamic of viral pneumonia?

A

Usually self-limiting, but dominated by secondary bacterial infection in severe cases

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19
Q

What group is most likely to get ill from CMV infection?

A

Immunocompromised people

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20
Q

What is the definition of sarcoidosis?

A

A granulomatous disorder of unknown cause affecting multple organs

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21
Q

What organ is mostly involved in sarcoidosis?

A

Lungs, but generally more often organs more exposed to the air

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22
Q

How often do sarcoidosis patients develop progressive disease?

A

1/3 of patients

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23
Q

What surrounds granulomas?

A

T cells

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24
Q

What is the epidemiological pattern of sarcoidosis?

A

High rate in scandinavia but low morbidity, lower rates in other places but worse prognosis

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25
Q

What is the prevalence of chronic development of sarcoidosis in non-LS patients?

A

50%, about 20% with fibrosis

26
Q

What are triggers of sarcoidosis?

A

Anorganic exposure, antigen exposure

27
Q

What drives a granuloma?

A

Ongoing cytokine production by T helper cells around a trigger

28
Q

What type of Th cells are present in pulmonary sarcoidosis?

A

Th17.1 cells

29
Q

What is a biomarker of patients who develop chronic sarcoidosis?

A

Higher Th17.1 proportion to other Th cells

30
Q

What is CTLA4?

A

A co-inhibitory receptor with higher affinity for CD80/CD86 than CD28

31
Q

What is the CTLA4 expression level in memory Th cells in sarcoidosis, and what type of Th cells?

A

Reduced, Tregs and Th17

32
Q

What does an increase in Th17 with reduced CTLA4 expression do?

A

Enhanced pro-inflammatory activity

33
Q

What is double trouble in sarcoidosis?

A

Reduced expression of CTLA4 in Tregs (less inhibition) and Th17 (enhanced pro-inflammatory response)

34
Q

What is a very pro-fibrotic cytokine?

A

TGFß

34
Q

What drug classes are associated with sarcoid-like reaction?

A

Checkpoint inhibitors

35
Q

What does JAK inhibition do?

A

Targets multiple cytokines involved in sarcoidosis, since JAK is a kinase in many pathways involved with cytokine signaling

36
Q

What is the most prominent type of asthma?

A

Type 2 asthma

37
Q

What are two ways to treat asthma?

A

Corticosteroids and Bronchodilators (ß2-agonists)

38
Q

What do corticosteroids target?

A

Almost every immune cell

39
Q

What do bronchodilators target?

A

Smooth muscle cells of the airway walls

40
Q

What are two down sides to corticosteroid use against asthma?

A

Can cause severe side effects, and sensitivity and response is highly dependent on disease phenotype

41
Q

What causes disease exacerbations in asthma?

A

Respiratory viral infections

42
Q

What is a doenside of ß2 agonist use?

A

It only targets one symptom and does not treat the inflammation

43
Q

What happens to tissues in chronic asthma?

A

Irreversible tissue remodelling, goblet cell hyperplasia

44
Q

What causes the rapid constriction of the airway in asthma?

A

Mast cell degranulation (histamine)

45
Q

What time of onset of asthma is Th2-associated and which is non-Th2 associated?

A

Childhood is Th2 (T2 high), usually allergy driven.

Adult is non-Th2 (T2 low), obesity and smoking associated, the later neutrophilic.

46
Q

What cytokines and adaptive and innate cells does T2 high asthma involve?

A

IL-4, IL-5, IL-13 and IL-9, Th2 and ILC2 and honestly almost every immune cell, even B cells

47
Q

What does IL-5 lead to?

A

Tissue eosinophilia

48
Q

What does IL-4 lead to?

A

IgE

49
Q

What do Th17 cytokines lead to in asthma?

A

T2 low asthma -> neutrophil recruitment

50
Q

What type of asthma is characterized by neutrophilic inflammation and involved IFNy and IL-17?

A

T2 low

50
Q

What cells are involved in T2 low asthma?

A

Th1, Th17, macrophages and ILC1

51
Q

What type of asthma is characterized by eosinophilic inflammation, type 2 cytokines and allergen-specific B cells and IgE?

A

T2 high

52
Q

What are alarmins?

A

Innate cytokines produced by epithelial cells that affect DCs and activate ILCs

53
Q

What do dendritic cells do in T2 high asthma?

A

Take up allergen, migrate to LN, active naive T cells, which proliferate and differentiate into Th2 cells.

54
Q

What are the two ways type 2 cytokine production is induced in T2 high asthma?

A

DCs to Th2 and alarmins to ILC2

55
Q

Where are neuroendocrine cells mostly found?

A

Bronchioles

56
Q

Where are goblet cells mainly found?

A

Trachea and bronchi, a bit in bronchioles

57
Q

Where are submucosal glands found?

A

Trachea and bronchi

58
Q

Where are club cells found?

A

Trachea, bronchi and bronchioles

59
Q

What do ILC2 cells respond to?

A

alarmins produced by the epithelium

60
Q

What cells do ILC2s interact with?

A

Almost everything you can think of

61
Q

What is IL-13 essential for?

A

DC activation and migration in protease-induced allergic airway inflammation

62
Q

What is a marker for activated ILC2s?

A

CD-45RO

63
Q

What is high levels of CD-45RO+ ILC2 associated with?

A

Asthma severity and unresponsiveness to corticosteroids

64
Q

What happens with chromatin in asthma patients?

A

It is open at genes encoding for ILC2

65
Q

What is the cytokine production pattern of CD8 T cells in severe asthma patients?

A

Type 2 cytokine production by CD8 T cells is highest in severe asthma patients

66
Q
A