PMID- 28972093
OWN - NLM
STAT- MEDLINE
DCOM- 20171026
LR  - 20180129
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 199
IP  - 9
DP  - 2017 Nov 1
TI  - The Cooperative Role of CD326(+) and CD11b(+) Dendritic Cell Subsets for a 
      Hapten-Induced Th2 Differentiation.
PG  - 3137-3146
LID - 10.4049/jimmunol.1601262 [doi]
AB  - Dendritic cells (DCs) play a critical role in directing immune responses. 
      Previous studies have identified a variety of DC subsets and elucidated their 
      context-dependent functions that parallel those of effector Th cell subsets. 
      However, little is known about the DC subsets responsible for differentiation of 
      Th2 cells governing allergic contact dermatitis. In this study, we sought to 
      determine the DC subset(s) that mediate Th2 priming in hapten-sensitized mice. We 
      induced hapten-specific Th2 differentiation by sensitizing the mice with a single 
      application of FITC dissolved in acetone:dibutyl phthalate, and traced the immune 
      cells responsible for inducing the Th2 differentiation process at the primary 
      stimulation, enabling us to track Th2 priming in vivo and to delete basophils and 
      specific DC subsets. Our analysis revealed that IL-4 was produced in vivo as 
      early as day 3 from CD4(+) T cells with a single application of FITC. Basophils, 
      despite producing IL-4 1 d earlier than T cells, were found to be dispensable for 
      Th2 differentiation. Instead, we demonstrated that CD326(+) dermal DCs and 
      Langerhans cells were redundantly required for FITC-induced Th2 differentiation 
      in vivo. Moreover, the cooperation of CD326(+) Langerhans cells and CD11b(+) DCs 
      differentiated naive T cells into Th2 cells in vitro. Collectively, our findings 
      highlight at least two DC subsets that play a critical role in polarizing naive 
      CD4(+) T cells to Th2 cells and support a two-hit model for Th2 differentiation.
CI  - Copyright (c) 2017 by The American Association of Immunologists, Inc.
FAU - Cho, Yuri
AU  - Cho Y
AD  - Department of Biological Sciences, Korea Advanced Institute of Science and 
      Technology, Daejeon 34141, Republic of Korea.
FAU - Kwon, Dohyeong
AU  - Kwon D
AD  - Department of Biological Sciences, Korea Advanced Institute of Science and 
      Technology, Daejeon 34141, Republic of Korea.
FAU - Kang, Suk-Jo
AU  - Kang SJ
AD  - Department of Biological Sciences, Korea Advanced Institute of Science and 
      Technology, Daejeon 34141, Republic of Korea suk-jo.kang@kaist.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171002
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (CD11b Antigen)
RN  - 0 (Epithelial Cell Adhesion Molecule)
RN  - 0 (Haptens)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Animals
MH  - CD11b Antigen/genetics/*immunology
MH  - Cell Differentiation/*drug effects/genetics/immunology
MH  - Epithelial Cell Adhesion Molecule/genetics/*immunology
MH  - Haptens/*pharmacology
MH  - Interleukin-4/genetics/immunology
MH  - Langerhans Cells/*immunology
MH  - Mice
MH  - Mice, Knockout
MH  - Th2 Cells/*immunology
EDAT- 2017/10/04 06:00
MHDA- 2017/10/27 06:00
CRDT- 2017/10/04 06:00
PHST- 2016/07/21 00:00 [received]
PHST- 2017/09/06 00:00 [accepted]
PHST- 2017/10/04 06:00 [pubmed]
PHST- 2017/10/27 06:00 [medline]
PHST- 2017/10/04 06:00 [entrez]
AID - jimmunol.1601262 [pii]
AID - 10.4049/jimmunol.1601262 [doi]
PST - ppublish
SO  - J Immunol. 2017 Nov 1;199(9):3137-3146. doi: 10.4049/jimmunol.1601262. Epub 2017 
      Oct 2.