Decline in TRECs with age and HIV infection Rob J. de Boer - - PowerPoint PPT Presentation

decline in trecs with age and hiv infection rob j de boer
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Decline in TRECs with age and HIV infection Rob J. de Boer - - PowerPoint PPT Presentation

Decline in TRECs with age and HIV infection Rob J. de Boer Theoretical Biology, UU Mette Hazenberg, Frank Miedema & Bas Dutilh 1 HIV infection: decrease in CD4 + T cell counts 2 Today: naive T cells Both CD4 + and CD8 + naive T cell counts


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Decline in TRECs with age and HIV infection Rob J. de Boer Theoretical Biology, UU Mette Hazenberg, Frank Miedema & Bas Dutilh

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HIV infection: decrease in CD4+ T cell counts

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Today: naive T cells Both CD4+ and CD8+ naive T cell counts decline Is this due to HIV infection of the thymus?

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Hazenberg et al., Blood, 2000 %Ki67 as a function of number of naive CD4+ T cells: At very low counts large fraction dividing naive T cells Similar data for naive CD8+ T cells

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Push Pull

Activation CD4 count Virus

+ − +

Activation CD4 count Virus

− −

Activation caused by homeostasis due to low counts? Or activation (due to virus) responsible for low counts?

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During therapy rapid normalization of division

  • : naive, triangle: CD27+ memory, squares: CD27− memory,

gray circles: total From: Hazenberg et al., Blood, 2000

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Counts recover much slower From: Hazenberg et al., Blood, 2000

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Push Pull

Activation CD4 count Thymus Virus

+ − + + −

Activation CD4 count Thymus Virus

− − + −

Or is infection of thymus responsible for low naive counts?

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TREC content declines one or two logs with age Age Total CD4 or CD8 (from: Douek et al., Nature, 1998).

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Thymectomy affects TREC content Age From: Douek et al., Nature, 1998.

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TREC content decreased in HIV-1+ patients Age → Evidence for decreased thymic output during HIV infection TREC content rapidly increases during therapy: → Evidence for recovery of thymic output during therapy.

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TREC model: Hazenberg et al., NM, 2000 In an attempt to resolve existing confusion on interpreting TREC data we developed a simple model: dN dt = σ(t) + [ρ(N) − δ(N)]N dT dt = cσ(t) − [δ(N) + δI]T for naive T cells N and the total TRECs T. c represents the TREC content of a RTE. Note that total TREC content is not diluted by division.

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Examples of functions

dN dt = σ(t) + [ρ(N) − δ(N)]N , dT dt = cσ(t) − [δ(N) + δI]T

Thymic production: σ(t) = σ0e−vt Density dependent renewal: ρ(N) = ρmax 1 + (N/h)k Density dependent death: δ(N) = δmin + (ǫN)m

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Average TREC content per naive T cell

dN dt = σ(t) + [ρ(N) − δ(N)]N , dT dt = cσ(t) − [δ(N) + δI]T

Define A ≡ T/N and derive that dA dt = σ(t) N (c − A) − [δI + ρ(N)]A ¯ A = c 1 + [δI + ρ(N)]N/σ(t)

  • no homeostasis, i.e., N ∝ σ(t), no decline in ¯

A

  • when δI = ρ(N) = 0, ¯

A = c

  • increasing division ρ(N) similar to decreasing σ(t)

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No homeostasis: no decrease in TREC content

dN dt = σ(t) + [ρ − δ]N , ¯ N = σ(t)/(δ − ρ)

¯ A = c 1 + [δI + ρ]/(δ − ρ) In the absence of density dependent renewal or death func- tions, the average TREC content will go to a steady state depending on renewal, death, and intracellular degradation. TREC data evidence for existence of homeostasis

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Density dependent renewal

✂ ✄ ☎ ✆

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N

(a)

k = 1 k = 2 k = 4

(c)

✂ ✄

(b)

c c/10 c/100 A

c A

c/10 c/100

  • 20
  • 40
  • 60
  • 80
  • 100
  • age
✁ ✂ ✄ ☎ ✆ ✝
  • 20
  • 40
  • 60
  • 80
  • 100
  • age
✁ ✂ ✄ ☎ ✆ ✝

δI = 0, δ is fixed

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Density dependent death

✂ ✄ ☎ ✆

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N

(a)

m = 0 m = 1 m = 2 m = 4

(c)

✂ ✄

(b)

c A

c/10 c/100

  • 20
  • 40
  • 60
  • 80
  • 100
  • age
✁ ✂ ✄ ☎ ✆ ✝
  • 20
  • 40
  • 60
  • 80
  • 100
  • age
✁ ✂ ✄ ☎ ✆ ✝

Needs either a small intracellular decay (δi) or low frequency

  • f division (ρ).

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HIV infection

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−4

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−3

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−2

10

−1

10 TRECs per naive T cell (A) 10

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Number of naive T cells

  • (B)

100

200

300

Time (days)

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−4

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−3

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−2

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−1

10 TRECs per naive T cell (C)

✄ ✁

100

200

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Time (days)

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Number of naive T cells

  • (D)

TRECs (solid line), Naive T cells (dashed line) At age 30 we set: (a) σ(t) = 0, (b) 10-fold increase δ (c) 10-fold increase ρ (d) 5-fold increase of ρ & δ

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Conclusion: many factors determine TREC content

  • opposite effect of thymus and division

→ effect of thymus is slow → effect of division is fast

  • increasing death increased TREC content

→ rapid changes in HIV-patients due to changes in division? Is this in agreement with data?

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Thymectomy

  • juvenile macaques: TRECs ≈ constant over a year
  • Sempowski, JI, 2001: thymectomy in Myasthenia gravis

patients affects TRECs only after > 3 months

  • σ = 0: nevertheless a decline in TREC content

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Division: Hazenberg et al., Nat. Med., 2000 %Ki67+ Naive T cells Douek, JI, 2001: similar negative correlation between TREC content and BrdU uptake

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Division: Hazenberg et al., submitted TREC content is reflecting replicative history black: healthy, gray HIV-1 infected patients

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Another confounding factor: TRECs/total T cells TREC content is typically measured per total CD4+ or to- tal CD8+ T cells, and is sometimes compared to division in whole population. Because the TREC content of naive T cells is much larger than that of memory cells, whereas their division rate is lower, such TREC measurements are easily confounded by changes in the ratios of naive/memory cells.

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Conclusion TREC content declines with age because thymic output de- creases. TREC content is not a quantitative measurement of thymic

  • utput because it is confounded by division and the (possible

density dependent) longevity of naive T cells. Lower TREC content in HIV patients cannot be used as ev- idence for impairment of thymic production. Whether or not HIV infection of thymus has an impact on the loss of naive T cells remains an open question.

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Not due to equilibrium assumption Fixed death rate: dN(t) dt = σe−vt − dN(t) , dT(t) dt = cσe−vt − dT(t) , has the solution: N(t) = σ d − v (e−vt − e−dt) , T(t) = cN(t) Hence the TREC content A ≡ T/N = c.

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TRECs are diluted by division

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