PMID- 16354183
OWN - NLM
STAT- MEDLINE
DCOM- 20060126
LR  - 20071114
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 125
IP  - 6
DP  - 2005 Dec
TI  - Immunology of the human nail apparatus: the nail matrix is a site of relative 
      immune privilege.
PG  - 1139-48
AB  - The nail apparatus is constantly exposed to environmental damage. It requires 
      effective immune responses to combat infection, while avoiding the loss of nail 
      production and regeneration by autoaggressive immunity. By immunohistology, we 
      define here previously unknown characteristics of the normal human nail immune 
      system (NIS). Compared with other regions of nail epithelium, human leukocyte 
      antigen (HLA)-A/B/C expression is prominently down regulated on both 
      keratinocytes and melanocytes of the proximal nail matrix (PNM), whereas HLA-G(+) 
      is upregulated here. Together with the expression of macrophage migration 
      inhibitory factor in PNM, this may serve to inhibit an natural killer (NK) cell 
      attack on major histocompatibility complex (MHC) class Ia-negative PNM. PNM also 
      displays strong immunoreactivity for potent, locally generated immunosuppressants 
      such as transforming growth factor-beta1, alpha-melanocyte stimulating hormone, 
      insulin-like growth factor-1, and adrenocorticotropic hormone, exhibits unusually 
      few CD1a(+), CD4(+), or CD8(+), NK, and mast cells. Finally, MHC class II and CD 
      209 expression on CD1a(+) cells in and around the PNM is reduced, indicating 
      diminished antigen-presenting capacity. Thus, the NIS strikingly differs from the 
      skin immune system, but shows intriguing similarities to the hair follicle immune 
      system, including the establishment of an area of relative immune privilege in 
      the PNM. This nail immune privilege may offer a relative safeguard against 
      autoimmunity. But, the localized intraepithelial defect of innate and adaptive 
      immunity in the PNM revealed here also may impede effective anti-infection 
      defense.
FAU - Ito, Taisuke
AU  - Ito T
AD  - Department of Dermatology, Hamamatsu University School of Medicine, Hamamatsu, 
      Japan. itoutai@hama-med.ac.jp
FAU - Ito, Natsuho
AU  - Ito N
FAU - Saathoff, Matthias
AU  - Saathoff M
FAU - Stampachiacchiere, Barbara
AU  - Stampachiacchiere B
FAU - Bettermann, Albrecht
AU  - Bettermann A
FAU - Bulfone-Paus, Sylvia
AU  - Bulfone-Paus S
FAU - Takigawa, Masahiro
AU  - Takigawa M
FAU - Nickoloff, Brian J
AU  - Nickoloff BJ
FAU - Paus, Ralf
AU  - Paus R
LA  - eng
GR  - AR40065/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Antigens, CD)
RN  - 0 (HLA-D Antigens)
SB  - IM
MH  - Antigens, CD/immunology
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - CD8-Positive T-Lymphocytes/immunology
MH  - Environment
MH  - Epithelial Cells/immunology
MH  - HLA-D Antigens/immunology
MH  - Humans
MH  - Infant
MH  - Killer Cells, Natural/immunology
MH  - Male
MH  - Mast Cells/immunology
MH  - Nails/cytology/*immunology/physiology
EDAT- 2005/12/16 09:00
MHDA- 2006/01/27 09:00
CRDT- 2005/12/16 09:00
PHST- 2005/12/16 09:00 [pubmed]
PHST- 2006/01/27 09:00 [medline]
PHST- 2005/12/16 09:00 [entrez]
AID - S0022-202X(15)32559-8 [pii]
AID - 10.1111/j.0022-202X.2005.23927.x [doi]
PST - ppublish
SO  - J Invest Dermatol. 2005 Dec;125(6):1139-48. doi: 
      10.1111/j.0022-202X.2005.23927.x.