An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic?Citation formats

  • External authors:
  • Gil Kaufman
  • Roberto d'Ovidio
  • Anis Kaldawy
  • Bedia Assy
  • Yehuda Ullmann
  • Amos Etzioni
  • Amos Gilhar

Standard

An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic? / Kaufman, Gil; d'Ovidio, Roberto; Kaldawy, Anis; Assy, Bedia; Ullmann, Yehuda; Etzioni, Amos; Paus, Ralf; Gilhar, Amos.

In: Experimental Dermatology, Vol. 19, No. 8, 08.2010, p. e347-e349.

Research output: Contribution to journalArticlepeer-review

Harvard

Kaufman, G, d'Ovidio, R, Kaldawy, A, Assy, B, Ullmann, Y, Etzioni, A, Paus, R & Gilhar, A 2010, 'An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic?', Experimental Dermatology, vol. 19, no. 8, pp. e347-e349. https://doi.org/10.1111/j.1600-0625.2010.01106.x

APA

Kaufman, G., d'Ovidio, R., Kaldawy, A., Assy, B., Ullmann, Y., Etzioni, A., Paus, R., & Gilhar, A. (2010). An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic? Experimental Dermatology, 19(8), e347-e349. https://doi.org/10.1111/j.1600-0625.2010.01106.x

Vancouver

Kaufman G, d'Ovidio R, Kaldawy A, Assy B, Ullmann Y, Etzioni A et al. An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic? Experimental Dermatology. 2010 Aug;19(8):e347-e349. https://doi.org/10.1111/j.1600-0625.2010.01106.x

Author

Kaufman, Gil ; d'Ovidio, Roberto ; Kaldawy, Anis ; Assy, Bedia ; Ullmann, Yehuda ; Etzioni, Amos ; Paus, Ralf ; Gilhar, Amos. / An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic?. In: Experimental Dermatology. 2010 ; Vol. 19, No. 8. pp. e347-e349.

Bibtex

@article{6571e93a4f4641e4abebdd8225a78e5c,
title = "An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic?",
abstract = "Natural killer (NK) cells have become a recent focus of interest in alopecia areata (AA) research. To further investigate their role in an established mouse model of AA, lesional skin from older C3H/HeJ mice with AA was grafted to young C3H/HeJ female mice, and NK cells were depleted by continuous administration of rabbit anti-asialo GM1. As expected, this significantly reduced the number of pure NK cells in murine skin, as assessed by NKp46 quantitative immunohistochemistry. Quite unexpectedly, however, the onset of hair loss in C3H/HeJ mice was accelerated, rather than retarded. NK cell depletion was accompanied by a significant increase in the number of perifollicular CD49b+T cells in the alopecic skin of anti-asialo GM1-treated mice. These findings underscore the need to carefully distinguish in future AA research between pure NK cells and defined subsets of CD49b+ lymphocytes, as they may exert diametrically opposed functions in hair follicle immunology and immunopathology. {\textcopyright} 2010 John Wiley & Sons A/S.",
keywords = "Alopecia Areata, Autoimmunity, CD49b+ cells, NK cells",
author = "Gil Kaufman and Roberto d'Ovidio and Anis Kaldawy and Bedia Assy and Yehuda Ullmann and Amos Etzioni and Ralf Paus and Amos Gilhar",
year = "2010",
month = aug,
doi = "10.1111/j.1600-0625.2010.01106.x",
language = "English",
volume = "19",
pages = "e347--e349",
journal = "Experimental Dermatology",
issn = "1600-0625",
publisher = "John Wiley & Sons Ltd",
number = "8",

}

RIS

TY - JOUR

T1 - An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic?

AU - Kaufman, Gil

AU - d'Ovidio, Roberto

AU - Kaldawy, Anis

AU - Assy, Bedia

AU - Ullmann, Yehuda

AU - Etzioni, Amos

AU - Paus, Ralf

AU - Gilhar, Amos

PY - 2010/8

Y1 - 2010/8

N2 - Natural killer (NK) cells have become a recent focus of interest in alopecia areata (AA) research. To further investigate their role in an established mouse model of AA, lesional skin from older C3H/HeJ mice with AA was grafted to young C3H/HeJ female mice, and NK cells were depleted by continuous administration of rabbit anti-asialo GM1. As expected, this significantly reduced the number of pure NK cells in murine skin, as assessed by NKp46 quantitative immunohistochemistry. Quite unexpectedly, however, the onset of hair loss in C3H/HeJ mice was accelerated, rather than retarded. NK cell depletion was accompanied by a significant increase in the number of perifollicular CD49b+T cells in the alopecic skin of anti-asialo GM1-treated mice. These findings underscore the need to carefully distinguish in future AA research between pure NK cells and defined subsets of CD49b+ lymphocytes, as they may exert diametrically opposed functions in hair follicle immunology and immunopathology. © 2010 John Wiley & Sons A/S.

AB - Natural killer (NK) cells have become a recent focus of interest in alopecia areata (AA) research. To further investigate their role in an established mouse model of AA, lesional skin from older C3H/HeJ mice with AA was grafted to young C3H/HeJ female mice, and NK cells were depleted by continuous administration of rabbit anti-asialo GM1. As expected, this significantly reduced the number of pure NK cells in murine skin, as assessed by NKp46 quantitative immunohistochemistry. Quite unexpectedly, however, the onset of hair loss in C3H/HeJ mice was accelerated, rather than retarded. NK cell depletion was accompanied by a significant increase in the number of perifollicular CD49b+T cells in the alopecic skin of anti-asialo GM1-treated mice. These findings underscore the need to carefully distinguish in future AA research between pure NK cells and defined subsets of CD49b+ lymphocytes, as they may exert diametrically opposed functions in hair follicle immunology and immunopathology. © 2010 John Wiley & Sons A/S.

KW - Alopecia Areata

KW - Autoimmunity

KW - CD49b+ cells

KW - NK cells

U2 - 10.1111/j.1600-0625.2010.01106.x

DO - 10.1111/j.1600-0625.2010.01106.x

M3 - Article

VL - 19

SP - e347-e349

JO - Experimental Dermatology

JF - Experimental Dermatology

SN - 1600-0625

IS - 8

ER -