PMID- 19440334
OWN - NLM
STAT- MEDLINE
DCOM- 20090806
LR  - 20221109
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 4
IP  - 5
DP  - 2009
TI  - MGL2 Dermal dendritic cells are sufficient to initiate contact hypersensitivity 
      in vivo.
PG  - e5619
LID - 10.1371/journal.pone.0005619 [doi]
LID - e5619
AB  - BACKGROUND: Dendritic cells (DCs) are the most potent antigen-presenting cells in 
      the mammalian immune system. In the skin, epidermal Langerhans cells (LCs) and 
      dermal dendritic cells (DDCs) survey for invasive pathogens and present antigens 
      to T cells after migration to the cutaneous lymph nodes (LNs). So far, functional 
      and phenotypic differences between these two DC subsets remain unclear due to 
      lack of markers to identify DDCs. METHODOLOGY/PRINCIPAL FINDINGS: In the present 
      report, we demonstrated that macrophage galactose-type C-type lectin (MGL) 2 was 
      exclusively expressed in the DDC subset in the skin-to-LN immune system. In the 
      skin, MGL2 was expressed on the majority (about 88%) of MHCII(+)CD11c(+) cells in 
      the dermis. In the cutaneous LN, MGL2 expression was restricted to 
      B220(-)CD8alpha(lo)CD11b(+)CD11c(+)MHCII(hi) tissue-derived DC. MGL2(+)DDC 
      migrated from the dermis into the draining LNs within 24 h after skin 
      sensitization with FITC. Distinct from LCs, MGL2(+)DDCs localized near the high 
      endothelial venules in the outer T cell cortex. In FITC-induced contact 
      hypersensitivity (CHS), adoptive transfer of FITC(+)MGL2(+)DDCs, but not 
      FITC(+)MGL2(-)DCs into naive mice resulted in the induction of FITC-specific ear 
      swelling, indicating that DDCs played a key role in initiation of immune 
      responses in the skin. CONCLUSIONS/SIGNIFICANCE: These results demonstrated the 
      availability of MGL2 as a novel marker for DDCs and suggested the contribution of 
      MGL2(+) DDCs for initiating CHS.
FAU - Kumamoto, Yosuke
AU  - Kumamoto Y
AD  - Laboratory of Cancer Biology and Molecular Immunology, Graduate School of 
      Pharmaceutical Sciences, the University of Tokyo, Tokyo, Japan.
FAU - Denda-Nagai, Kaori
AU  - Denda-Nagai K
FAU - Aida, Satoshi
AU  - Aida S
FAU - Higashi, Nobuaki
AU  - Higashi N
FAU - Irimura, Tatsuro
AU  - Irimura T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090519
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antigens, CD)
RN  - 0 (Asialoglycoproteins)
RN  - 0 (CD11b Antigen)
RN  - 0 (CD11c Antigen)
RN  - 0 (CD8 Antigens)
RN  - 0 (CD8alpha antigen)
RN  - 0 (Clec10a protein, mouse)
RN  - 0 (DEC-205 receptor)
RN  - 0 (Lectins, C-Type)
RN  - 0 (MGL2 protein, mouse)
RN  - 0 (Membrane Proteins)
RN  - 0 (Minor Histocompatibility Antigens)
RN  - 0 (Receptors, Cell Surface)
SB  - IM
MH  - Animals
MH  - Antigens, CD/metabolism
MH  - Asialoglycoproteins/metabolism
MH  - CD11b Antigen/metabolism
MH  - CD11c Antigen/metabolism
MH  - CD8 Antigens/metabolism
MH  - Cell Movement/physiology
MH  - Dermatitis, Contact/*immunology
MH  - Flow Cytometry
MH  - Langerhans Cells/*immunology/metabolism
MH  - Lectins, C-Type/*metabolism
MH  - Membrane Proteins/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Minor Histocompatibility Antigens
MH  - Receptors, Cell Surface/metabolism
MH  - Skin/*immunology/metabolism
PMC - PMC2680031
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2009/05/15 09:00
MHDA- 2009/08/07 09:00
PMCR- 2009/05/19
CRDT- 2009/05/15 09:00
PHST- 2008/12/18 00:00 [received]
PHST- 2009/04/14 00:00 [accepted]
PHST- 2009/05/15 09:00 [entrez]
PHST- 2009/05/15 09:00 [pubmed]
PHST- 2009/08/07 09:00 [medline]
PHST- 2009/05/19 00:00 [pmc-release]
AID - 08-PONE-RA-07838R1 [pii]
AID - 10.1371/journal.pone.0005619 [doi]
PST - ppublish
SO  - PLoS One. 2009;4(5):e5619. doi: 10.1371/journal.pone.0005619. Epub 2009 May 19.