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Age-associated defect in human TLR-1/2 function.

David van Duin1, Subhasis Mohanty, Venetta Thomas

  • 1Section of Infectious Disease, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|January 5, 2007
PubMed
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Aging significantly impairs Toll-like receptor 1/2 (TLR1/2) function in humans, reducing cytokine production. This defect, linked to lower TLR1 expression, may increase infection risk and reduce vaccine efficacy in older adults.

Area of Science:

  • Immunology
  • Gerontology

Background:

  • Toll-like receptor (TLR) function is crucial for innate immunity.
  • The impact of aging on human TLR function is not fully understood.

Purpose of the Study:

  • To investigate the effects of aging on human TLR function and expression in monocytes.

Main Methods:

  • Assessed TLR function and cytokine production (TNF-alpha, IL-6) in monocytes from young and older adults using flow cytometry.
  • Analyzed TLR1 and TLR2 surface expression.
  • Utilized multivariable mixed-effect models.

Main Results:

  • Older adults exhibited a significant defect in TLR1/2-induced TNF-alpha and IL-6 production compared to young controls.
  • This defect correlated with decreased baseline TLR1 surface expression, but not TLR2.

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  • Other TLR-induced cytokine production remained largely intact in older adults.

    • Conclusions:

    • Aging impairs human TLR1/2 signaling, potentially due to reduced TLR1 expression.
    • This diminished immune response may contribute to increased susceptibility to infections and reduced vaccine effectiveness in the elderly.