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Dyslipidemia associated with atherosclerotic disease systemically alters dendritic cell mobilization

Véronique Angeli1, Jaime Llodrá, James X Rong

  • 1Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

Immunity
|October 16, 2004
PubMed

Insights

Changes in lipid profiles associated with atherosclerosis activate skin dendritic cells (DCs), causing inflammation and impairing their migration. High-density lipoprotein (HDL) and PAFAH restore DC function, crucial for immune response.

Area of Science:

  • Immunology
  • Dermatology
  • Cardiovascular Science

Background:

  • Dyslipidemia, characterized by high LDL and/or low HDL, is a risk factor for atherosclerosis.
  • Altered lipid profiles are common in systemic lupus erythematosus, rheumatoid arthritis, and psoriasis.
  • Atherosclerosis-related lipid changes impact immune cell function.

Purpose of the Study:

  • To investigate the effect of atherosclerotic lipid profiles on skin dendritic cells (DCs) and their migration.
  • To identify mechanisms underlying impaired DC migration in the context of dyslipidemia.
  • To explore potential therapeutic interventions for restoring DC function.

Main Methods:

  • Murine models with altered lipid profiles mimicking atherosclerotic disease.
  • Assessment of dendritic cell activation, dermal inflammation, and lymph node hypertrophy.
  • Analysis of DC migration to lymph nodes and immune cell priming.
  • Investigated the role of platelet-activating factor (PAF) and oxidized LDL in DC migration.
  • Evaluated the effect of HDL and PAFAH on DC function.

Main Results:

  • Atherosclerotic lipid profiles activated skin DCs, promoting local inflammation and lymph node enlargement.
  • DC migration to lymph nodes was paradoxically impaired, suppressing immune priming.
  • Inhibitory signals from PAF or oxidized LDL mimetic were identified as causes of impaired migration.
  • HDL and HDL-associated PAFAH restored normal DC migration and immune priming.
  • PAFAH inactivates PAF and oxidized LDL, thereby normalizing DC function.

Conclusions:

  • Atherosclerotic dyslipidemia can sequester activated DCs in the skin, exacerbating local inflammation.
  • Impaired DC migration due to lipid changes compromises essential immune surveillance functions.
  • HDL and PAFAH play a critical role in maintaining a functional DC compartment by regulating PAF and oxidized LDL.
  • Restoring DC function via HDL or PAFAH may be a therapeutic strategy for inflammatory and autoimmune diseases with dyslipidemia.

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