PMID- 10422564
OWN - NLM
STAT- MEDLINE
DCOM- 19990914
LR  - 20171116
IS  - 0367-6102 (Print)
IS  - 0367-6102 (Linking)
VI  - 74
IP  - 3
DP  - 1999 May
TI  - [Analysis of contact hypersensitivity response in human monocyte chemoattractant 
      protein (MCP)-1 transgenic mice].
PG  - 199-216
AB  - Epidermal Langerhans cells (LC) belong to the dendritic cell lineage and 
      represent the major antigen-presenting cells (APC) within the skin. The molecular 
      mechanisms responsible for LC migration to the skin have not fully been defined. 
      MCP-1 is a cytokine of C-C chemokine subfamily that is chemotactic in vitro for 
      monocytes, memory T cells and dendritic cells. In the present study, to examine 
      the roles of LC and MCP-1 in hapten-induced contact hypersensitivity response 
      (CHR), we utilized human MCP-1 transgenic mice (hMCP-1 Tgm) that produce 
      constitutively high levels of hMCP-1 in the sera. Following DNFB sensitization, 
      enhancement of CHR was demonstrated in Tgm as compared with CHR in non-Tgm at the 
      entire period examined. Anti-hMCP-1 antibody significantly inhibited the 
      DNFB-included CHR in Tgm. For analysis of the mechanisms underlying the enhanced 
      CHR, migration and activation of LC were examined in Tgm and non-Tgm. The number 
      of LC in the Tgm skin was within a normal range. However, the Tgm showed an 
      accumulation of NLDC-145+ cells in the draining lymph nodes (DLN) 24 h after DNFB 
      sensitization. When Tgm and non-Tgm were treated with FITC, the number of 
      FITC+NLDC-145+ cells was larger in Tgm DLN than that in non-Tgm DLN 24 h after 
      FITC application. Moreover, administration of recombinant hMCP-1 to BALB/c mice 
      led to an increase of FITC+NLDC-145+ cells in the DLN. In addition, 12 h after 
      application of FITC, LC in the epidermal sheets of Tgm increased in size and 
      expressed high levels of I-Ad as compared with those of non-Tgm. Expression of 
      B7-1 in 24h-cultured LC of BA LB/c mice was augmented by addition of recombinant 
      hMCP-1 in a dose-dependent manner. These findings suggest that MCP-1 accelerates 
      LC migration from epidermis into the DLN and up-regulates I-Ad and B7-1 
      expressions on the LC, which eventually enhances CHR.
FAU - Mizumoto, N
AU  - Mizumoto N
AD  - Department of Dermatology, Hokkaido University School of Medicine, Sapporo, 
      Japan.
LA  - jpn
PT  - Journal Article
PL  - Japan
TA  - Hokkaido Igaku Zasshi
JT  - [Hokkaido igaku zasshi] The Hokkaido journal of medical science
JID - 17410290R
RN  - 0 (B7-1 Antigen)
RN  - 0 (Chemokine CCL2)
RN  - D241E059U6 (Dinitrofluorobenzene)
SB  - IM
MH  - Animals
MH  - Antigen-Presenting Cells/metabolism/*physiology
MH  - B7-1 Antigen/metabolism
MH  - Cell Movement
MH  - Chemokine CCL2/genetics/*physiology
MH  - Dermatitis, Contact/*immunology
MH  - Dinitrofluorobenzene/immunology
MH  - Humans
MH  - Langerhans Cells/metabolism/*physiology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Transgenic
MH  - T-Lymphocytes/immunology
MH  - Up-Regulation
EDAT- 1999/07/28 00:00
MHDA- 1999/07/28 00:01
CRDT- 1999/07/28 00:00
PHST- 1999/07/28 00:00 [pubmed]
PHST- 1999/07/28 00:01 [medline]
PHST- 1999/07/28 00:00 [entrez]
PST - ppublish
SO  - Hokkaido Igaku Zasshi. 1999 May;74(3):199-216.