Ultraviolet B radiation induces a transient appearance of IL-4+ neutrophils, which support the development of Th2 responses

J Immunol. 2002 Apr 15;168(8):3732-9. doi: 10.4049/jimmunol.168.8.3732.

Abstract

UVB irradiation can cause considerable changes in the composition of cells in the skin and in cutaneous cytokine levels. We found that a single exposure of normal human skin to UVB induced an infiltration of numerous IL-4(+) cells. This recruitment was detectable in the papillary dermis already 5 h after irradiation, reaching a peak at 24 h and declining gradually thereafter. The IL-4(+) cells appeared in the epidermis at 24 h postradiation and reached a plateau at days 2 and 3. The number of IL-4(+) cells was markedly decreased in both dermis and epidermis at day 4, and at later time points, the IL-4 expression was absent. The IL-4(+) cells did not coexpress CD3 (T cells), tryptase (mast cells), CD56 (NK cells), and CD36 (macrophages). They did coexpress CD15 and CD11b, showed a clear association with elastase, and had a multilobed nucleus, indicating that UVB-induced infiltrating IL-4(+) cells are neutrophils. Blister fluid from irradiated skin, but not from control skin, contained IL-4 protein as well as increased levels of IL-6, IL-8, and TNF-alpha. In contrast to control cultures derived from nonirradiated skin, a predominant type 2 T cell response was detected in T cells present in primary dermal cell cultures derived from UVB-exposed skin. This type 2 shift was abolished when CD15(+) cells (i.e., neutrophils) were depleted from the dermal cell suspension before culturing, suggesting that neutrophils favor type 2 T cell responses in UVB-exposed skin.

MeSH terms

  • Adult
  • Blister / immunology
  • Blister / metabolism
  • Blister / pathology
  • Cells, Cultured
  • Dermis / cytology
  • Dermis / immunology
  • Dermis / metabolism
  • Dermis / radiation effects
  • Dose-Response Relationship, Radiation
  • Humans
  • Immunomagnetic Separation
  • Interleukin-4 / biosynthesis*
  • Interleukin-4 / radiation effects
  • Lewis X Antigen / biosynthesis
  • Neutrophil Infiltration / immunology
  • Neutrophil Infiltration / radiation effects*
  • Neutrophils / immunology*
  • Neutrophils / metabolism
  • Neutrophils / radiation effects*
  • Th2 Cells / immunology*
  • Th2 Cells / metabolism
  • Th2 Cells / radiation effects*
  • Time Factors
  • Ultraviolet Rays*

Substances

  • Lewis X Antigen
  • Interleukin-4