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Maintenance of Hair Follicle Immune Privilege Is Linked to Prevention of NK Cell Attack  Taisuke Ito, Natsuho Ito, Matthias Saatoff, Hideo Hashizume, Hidekazu.

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Presentation on theme: "Maintenance of Hair Follicle Immune Privilege Is Linked to Prevention of NK Cell Attack  Taisuke Ito, Natsuho Ito, Matthias Saatoff, Hideo Hashizume, Hidekazu."— Presentation transcript:

1 Maintenance of Hair Follicle Immune Privilege Is Linked to Prevention of NK Cell Attack 
Taisuke Ito, Natsuho Ito, Matthias Saatoff, Hideo Hashizume, Hidekazu Fukamizu, Brian J. Nickoloff, Masahiro Takigawa, Ralf Paus  Journal of Investigative Dermatology  Volume 128, Issue 5, Pages (May 2008) DOI: /sj.jid Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

2 Figure 1 Perifollicular NK cells and T lymphocytes are scarce in normal skin, but accumulate around HFs in lesional skin of AA patients. In healthy controls, CD8+ T cells, CD4+ T cells, and CD56+ cells (NK cells) are rarely seen around anagen HFs (a–c, respectively; APAAP immunohistology). (d–f) However, these cells prominently infiltrate in and around HFs in AA lesions. (i) The number of infiltrating CD56+ cells in and around AA lesions (17.3±1.03) is significantly higher than around normal anagen (2±0.3) or catagen (2.3±0.19) HFs (P<0.01). The same is true for (g) CD4+ or (h) CD8+ T cells. Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

3 Figure 2 AA-HFs prominently and aberrantly express the NK cell activator MICA. (a) MICA IR was found to be largely absent in healthy control skin, with the exception of some MICA IR in the hair matrix of some normal anagen HFs. (b) Instead, MICA IR was massive throughout lesional skin HF from AA patients and was seen prominently in the inner root sheath, ORS, and connective tissue sheath. The MI of MICA IR was analyzed using ImageJ software. (c) The MI in the ORS was significantly lower in normal human scalp skin (27.82±3.33) than in lesional AA skin (115.0±2.2) (P<0.01), while there was no significant difference in hair matrix (control: 71.4±8.28, AA: 87.6±0.38). (d and e) NKG2D+ NK cells and CD8+ lymphocytes, which recognize MICA, prominently accumulate around HFs in AA (note the perifollicular aggregation of NKG2D+/CD56+ and NKG2D+/CD8+ cells around lesional AA-HFs). Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

4 Figure 3 MIF is strongly expressed on the proximal inner root sheath and matrix cells of anagen HFs. HF cells are compared with epidermal cells in healthy control skin (a by avidin–biotin complex and b by EnVision). (a) Avidin–biotin complex immunohistochemistry revealed strong IR of MIF in the proximal inner root sheath and matrix keratinocytes of anagen HFs in healthy control skin. (b) In contrast, MIR IR was greatly reduced in lesional AA HFs (not shown) and even a considerably more sensitive immunostaining technique (EnVision) revealed only weak MICA-associated IR in lesional AA-HFs (c). Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

5 Figure 4 In AA patients, the NK cell-activating receptor NKG2D is significantly upregulated on CD56+ NK cells and CD8+ T cells. By flow cytometry, peripheral blood CD56+ NK cells and CD8+ T cells of AA patients show significantly higher MI of NKG2D compared to normal controls (P<0.01, P<0.05, respectively): NKG2D MI is 90.06±19.06 on NK cells (a and b) and 97.50±9.72 on CD8+ T cells (c and d) in normal control and 90.92±30.13 on NK cells (a and b) and 69.61±9.15 on CD8+ T cells (c and d) in AD patients. In AA patients, MI is 213.5±23.63 on NK cells (a and b) and 183.5±9.15 on CD8+ T cells (c and d). Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

6 Figure 5 IFN-γ treatment potently upregulates NKG2D expression on NK cells of healthy controls to the abnormally high constitutive expression level of AA patients. (a) NKG2D MI is strongly upregulated by 100 and 1000IUml−1 IFN-γ in vitro. (b) HFs from AA patients show a high constitutive NKG2D MI, which is comparable to that induced by 100IUml−1 IFN-γ in normal controls, and cannot be further upregulated by IFN-γ administration. (c) Real-time PCR reveals up-regulation of NKG2D by IFN-γ. Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

7 Figure 6 NKG2C expression is significantly higher on NK cells in AA patients compared to normal controls and patients with atopic dermatitis. The MI of another NK-activating receptor, NKG2C, is significantly higher on NK cells from PBMCs in AA patients (81.89±5.6) compared to normal controls (39.22±14.7) and AD patients (42.46±2.76) (P<0.05). Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

8 Figure 7 NK cell expression of the inhibitory receptor, KIR-2D2/2D3, is lower in AA patients. The ratio of KIR-2D2/2D3−CD56+ cells/KIR-2D2/2D3+CD56+ cells is significantly higher in AA patients (3.85±0.18) compared to normal controls (2.58±0.12) (P<0.05) and patients with atopic dermatitis (2.43±0.27) (P<0.05). Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

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