B15: mucosal immunity 3 Flashcards

1
Q

What are the key immune defences in the urogenital tract (UGT)?

A

πŸ‘©β€βš•οΈ Female & πŸ‘¨β€βš•οΈ Male immune systems protect against STIs like HPV and HIV

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2
Q

What are the main parts of the respiratory tract (RT) immune system?

A

πŸ”Ό Upper RT (nose, sinuses) & πŸ”½ Lower RT (lungs, alveoli).

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3
Q

Name two common viruses of the RT.

A

🀧 Influenza (flu) and 🦠 SARS-CoV-2 (COVID-19).

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4
Q

Which viruses have effective vaccines?

A

βœ… Poliovirus πŸ’‰, HPV 🧬, COVID-19 πŸ’‰.

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5
Q

Which viruses have only moderately effective vaccines?

A

⚠️ Rotavirus 🦠, Flu (Influenza) 🀧.

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6
Q

Which virus has no vaccine?

A

❌ HIV 🦠.

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7
Q

Match the virus to its genetic material:
SARS-CoV
Influenza
HPV
Poliovirus
HIV
Rotavirus

A

SARS-CoV 🧬: ssRNA
Influenza 🦠: ssRNA segmented
HPV 🧬: dsDNA
Poliovirus 🦠: ssRNA
HIV 🦠: mRNA
Rotavirus 🦠: dsRNA

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8
Q

What is the main type of immunoglobulin in the respiratory and urogenital tracts?

A

πŸ›‘οΈ IgG + IgA (99% in RT, 98% in UGT).

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9
Q

How does the UGT immune system adapt to balance defence and reproduction?

A

πŸ›‘οΈ Protects against STIs
🦠 Differentiates microbiota from pathogens
🐣 Tolerates reproduction:
🧬 Sperm must fertilise the egg
🀰 Fetus must not be rejected

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10
Q

🚫What’s missing in the UGT immune system (unlike other mucosal sites)?

A

🚫No MALT or M-cells (an adaptation to support reproduction).

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11
Q

🚫What antibody can cause infertility in both men and women?

A

🚫πŸ§ͺ Anti-sperm antibodies β€” linked to 12% of male infertility cases.

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12
Q

What’s the difference between transudation and exudation?

A

πŸ”„ Transudation: Plasma filtrate flows across epithelium (carries IgG).
🌊 Exudate: Fluid from tissue damage/inflammation.

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13
Q

What can cause tissue damage in the vaginal mucosa?

A

🦠 Microbes: HSV, bacteria, fungi
πŸ”₯ Irritants: Spermicides
πŸ’₯ Physical damage: Contact during intercourse, menstrual changes

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14
Q

How does the adaptive immune system fight infections in vaginal mucosa?

A

🧬 CD4+ T-cells πŸ”₯ block viral replication (IFNΞ³).
🧬 CD8+ T-cells πŸ”₯ kill infected cells.
πŸ›‘οΈ IgG from both local production & bloodstream block virus entry.

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15
Q

Why is there an effective vaccine for HPV but not HIV?

A

βœ… HPV: Slow mutations, strong systemic response (IgG).
❌ HIV: Fast mutations, weak antibody response, πŸ› οΈ HAART treatment controls the virus but doesn’t cure it.

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16
Q

How does the RT defend itself from infection?

A

πŸ›‘οΈ Mechanical barriers (nose hairs, mucus)
🧼 Clearance mechanisms (cilia sweep away particles)
🦠 Microbiota
πŸ› οΈ Innate & adaptive immune cells

17
Q

What are the 3 main sections of the respiratory tract?

A

πŸ”Ό Upper airways: NALT (nose, sinuses, pharynx)
πŸ› οΈ Central airways: BALT (trachea, bronchi – present mainly in children)
πŸ”½ Lower airways: Alveoli

18
Q

What’s the difference between antigenic shift and drift?

A

πŸ”„ Antigenic shift: Major change due to gene reassortment (big mutation).
πŸ”„ Antigenic drift: Minor changes from small mutations over time (annual flu).

19
Q

What is a cytokine storm?

A

πŸŒͺ️ Overactive immune response β†’ massive IL-6 cytokine release
πŸ› οΈ Causes tissue damage and inflammation, leading to severe outcomes (e.g., COVID-19 pneumonia).

20
Q

What are the main routes of HIV transmission?

A

πŸ† Sexual transmission: Vaginal, anal, oral
πŸ’‰ Blood-to-blood: Needles, transfusions (rare now)
🀱 Mother-to-child: Birth, breastfeeding
πŸ› οΈ Mucosal exposure: Microtears in genital/rectal mucosa allow HIV entry

21
Q

How does HIV invade the body after mucosal exposure?

A

1️⃣ Crosses mucosal epithelium β€” via microabrasions or direct transport by dendritic cells
2️⃣ Infects CD4+ T cells β€” uses CCR5 or CXCR4 coreceptors
3️⃣ Spreads systemically β€” travels to lymph nodes, blood, organs

22
Q

What makes HPV an easier vaccine target than HIV?

A

βœ… HPV DNA is stable (HIV mutates rapidly)
βœ… HPV stays local (HIV spreads to immune cells)
βœ… HPV doesn’t integrate into DNA early (HIV integrates quickly)
βœ… HPV immune response is strong (HIV evades immunity)

23
Q

Why do HIV vaccines fail so far?

A

πŸ”„ HIV mutates too fast
πŸ›‘οΈ Weak antibody response β€” HIV hides in cells
🧬 Glycan shield β€” Sugar coating blocks antibodies
πŸ”₯ Targets immune cells (CD4) β€” The cells meant to fight it get infected

24
Q

How does HAART (Highly Active Antiretroviral Therapy) work against HIV?

A

πŸ’Š Reverse transcriptase inhibitors: Block viral RNA β†’ DNA conversion
πŸ’Š Protease inhibitors: Stop new virus assembly
πŸ’Š Integrase inhibitors: Prevent virus from integrating into host DNA
πŸ’Š Entry inhibitors: Block virus binding to CD4+ cells

25
Q

What’s a potential breakthrough strategy for HIV vaccines?

A

πŸ› οΈ Broadly neutralising antibodies (bNAbs) β€” target conserved parts of HIV
🧬 mRNA vaccines β€” like COVID-19, may boost immune response
πŸ”¬ T-cell vaccines β€” train CD8+ cytotoxic T-cells to kill infected cells faster

26
Q

what is transudation in the urogenital tract

A

the flow of plasma filtrate in the epithelium, allowing immune elements like IgG to pass through - a potential defence mechanism

27
Q

What is exudation?

A

fluid build-up caused by tissue leakage due to inflammation or cell damage.

28
Q

What are some causes of tissue damage in the vaginal mucosa?

A

Microbial factors: Viruses (e.g., HSV), bacterial infections, Candida overgrowth

Physical factors: Sexual activity or tools

Menstrual cycle: Tissue changes throughout the cycle

Chemical irritants: Spermicides like nonoxynol-9 disrupt epithelial membranes

29
Q

How do antibodies block viral entry in vaginal mucosa? πŸ›‘

A

Immunoglobulins (IgG, SIgA, mIgA) from both local and systemic sources block virus entry.

30
Q

: What immune cells are found in the trachea and alveoli? 🦠

A

Trachea: Ciliated epithelial cells (EC), goblet cells, dendritic cells, macrophages, CD4+, CD8+, B-cells (SIgA)

Alveoli: Type I & II epithelial cells, dendritic cells, macrophages, T-cells

31
Q

What cytokine is heavily linked to cytokine storms and sepsis? πŸ”₯

A

IL-6 β€” high levels were observed in COVID-19 patients who didn’t recover.