Week 4.1 Prevents immune amnesia → maintains protection against other diseases.

What happens after the first exposure to a pathogen?

Naïve B and T cells are activated, differentiate into effector cells, clear the pathogen, and some become long-lived memory cells.

What characterizes the primary immune response?

Slow onset, low antibody concentration; first IgM then IgG. Limited affinity.

What happens in the secondary immune response?

Faster, stronger reaction dominated by IgG with higher affinity due to affinity maturation.

What is the role of AID in B cells?

Activation-Induced Deaminase drives isotype switching and somatic hypermutation in the germinal center.

Why is T cell help crucial for B cell maturation?

CD4⁺ T helper cells provide CD40–CD40L signals and cytokines; without them, no high-affinity or isotype-switched antibodies form.

Which antibody appears first in a primary infection?

IgM.

Which antibody dominates the secondary and tertiary responses?

IgG, with higher affinity each time.

What ensures long-term antibody stability?

Long-lived plasma cells in bone marrow that continuously secrete antibodies.

Where are naïve T cells found and how do they migrate?

They circulate through lymphoid organs using receptors CD62L (L-selectin) and CCR7.

What are characteristics of naïve T cells?

Resting, no cytokine production, no effector molecules, very low numbers.

What happens after activation of naïve T cells?

They become effector T cells, lose CD62L/CCR7, migrate to tissues, and express interferon-γ, granzyme B, and FasL.

What happens after the effector phase?

Some cells transition into memory T cells that persist long-term and react quickly upon reactivation.

Wat zijn de drie hoofdtypen geheugen-T-cellen?

Central Memory (Tcm), Effector Memory (Tem) en Tissue-Resident Memory (Trm).

Waar bevinden Central Memory T-cellen (Tcm) zich en wat doen ze?

Ze circuleren door de lymfeklieren en zorgen voor langdurige bescherming door snel nieuwe effectorcellen te maken bij herinfectie.

Waar bevinden Effector Memory T-cellen (Tem) zich en wat is hun functie?

Ze bevinden zich in perifere weefsels en reageren direct door cytokines en cytotoxische stoffen te produceren. Ze leven korter.

Wat is de rol van Tissue-Resident Memory T-cellen (Trm)?

Ze blijven permanent in één weefsel, zoals de huid of longen, en zorgen voor directe lokale bescherming.

Wat zijn Stem Cell–like Memory T-cellen (Tscm)?

Een subtype van Tcm met stamcelachtige eigenschappen; ze delen heel traag maar blijven extreem lang leven.

Wat zijn TEMRA-cellen?

Sterk gedifferentieerde T-cellen die opnieuw CD45RA tot expressie brengen, vaak gezien bij chronische infecties zoals CMV.

Welke receptoren gebruiken naïeve en centrale geheugen-T-cellen om lymfeklieren binnen te gaan?

CD62L (L-selectin) en CCR7.

Waarom zijn er verschillende subtypen geheugen-T-cellen?

Ze zorgen samen voor snelle, langdurige en weefsel-specifieke bescherming tegen herinfecties.

What was observed in newborns vs adults?

Newborns: all influenza-specific T cells were naïve (CD45RA⁺).
Adults: mostly central memory T cells.

How does antigen-specific T cell frequency change with age?

Increases tenfold from newborns to adults due to accumulation of memory.

What does this study illustrate?

Memory T cells are stable and long-lasting throughout life.

What type of virus is measles?

Single-stranded, negative-sense RNA virus, enveloped.

What is the main uptake receptor for measles?

SLAM/CD150.

What are its main host and contagious properties?

Humans only; highly contagious (R₀ = 12–18, virus remains airborne for up to 2 hours).

Which cells are infected first?

Alveolar macrophages and dendritic cells (express CD150).

What happens after initial infection?

Virus spreads via lymphocytes throughout the body (viremia).

Which cells produce most virus particles?

Lung epithelial cells — major source for transmission.

In short, what is the infection sequence?

Myeloid cells → lymphocytes → systemic spread → lung epithelium → transmission.

What is “immune amnesia”?

Loss of pre-existing immune memory after measles infection.

Which cells are primarily targeted?

Memory T cells and B cells expressing CD150 (SLAM).

What happens when these cells are destroyed?

Loss of immune memory → reduced antibody levels for past infections.

What is the consequence for the immune system?

It must rebuild immunity from scratch; increased vulnerability to other infections.

Why does measles immunity stay strong while others disappear?

The empty “memory compartment” is refilled by measles-specific lymphocytes.

How long does this immunosuppression last?

Months to years after recovery.

What is SSPE?

A rare, fatal brain disease that appears years after measles infection.

What causes SSPE?

Mutated measles virus persisting in neurons, astrocytes, and oligodendrocytes.

How does the virus spread in SSPE?

Through cell-to-cell fusion without producing full virus particles.

What are the symptoms?

Behavioral changes, dementia, myoclonic jerks, seizures → fatal within a few years.

Who is most at risk?

Children infected before age 1.

Can SSPE result from vaccination?

No, only from wild-type virus.

What vaccine prevents measles?

The MMR vaccine (Measles, Mumps, Rubella).

When is it given and why not earlier?

At 14 months — earlier maternal antibodies would neutralize it, so the child immune systeem doesnt have the chance to make memory cells. an other resean is because the immune system of the child isnt develept well enaugh: immature immunity

What is the herd immunity threshold for measles?

~95 % vaccination coverage.

Why is this threshold so high?

Measles is extremely contagious (R₀ = 12–18).

What happens if coverage drops below 95 %?

Outbreaks occur (as seen in the UK, Samoa, Texas 2025).

Who depends on herd immunity?

Immunosuppressed individuals who cannot be vaccinated.

How does measles vaccination indirectly save lives?

Prevents immune amnesia → maintains protection against other disease