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An Efficient and High Yield Method for Isolation of Mouse Dendritic Cell Subsets
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Dendritic cell function at low physiological temperature.

Oscar Hammarfjord1, Robert P A Wallin

  • 1Center for Infectious Medicine, F59, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden.

Journal of Leukocyte Biology
|July 24, 2010
PubMed
Summary
This summary is machine-generated.

Skin temperature affects dendritic cell (DC) function. While some DC functions remain normal at 28°C, others like NO production and T cell activation are impaired, impacting adaptive immunity.

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Area of Science:

  • Immunology
  • Cell Biology
  • Dendritic Cell Biology

Background:

  • Skin temperature is lower than core body temperature and varies with environmental conditions.
  • Dendritic cells (DCs) are abundant in the skin, but their function at lower physiological temperatures is not well understood.

Purpose of the Study:

  • To investigate the functional capacity of dendritic cells (DCs) at a lower temperature (28°C) compared to standard physiological temperature (37°C).
  • To determine how temperature affects DC functions relevant to innate and adaptive immunity.

Main Methods:

  • Assessed DC phagocytosis, macropinocytosis, and Toll-like receptor 4 (TLR-4) signaling pathways (MAPK, TNF, NO production) at 28°C.
  • Evaluated collagen degradation, DC migration (through matrigel-coated and non-coated transwell inserts), and expression of co-stimulatory molecules (CD86, CD40) at 28°C.
  • Compared antigen processing, presentation on MHC class II, and T cell activation by DCs cultured at 28°C versus 37°C.

Main Results:

  • DCs maintained phagocytosis and macropinocytosis at 28°C, though TLR-4 signaling kinetics were delayed.
  • TLR-4-induced nitric oxide (NO) production was severely compromised at 28°C.
  • Collagen degradation and migration were reduced, while CD40 upregulation was suppressed; CD86 upregulation and MHC class II antigen presentation were unaffected.
  • DCs activated at 28°C showed reduced capacity to activate T cells at 37°C compared to those activated at 37°C.

Conclusions:

  • Lower skin temperatures differentially regulate DC functions, impacting their role in adaptive immunity.
  • Impaired NO production and T cell activation at 28°C suggest reduced immune surveillance and response in cooler skin conditions.
  • DCs retain some functions but exhibit significant deficits in others at 28°C, highlighting temperature-dependent immune modulation.