PMID- 19879735
OWN - NLM
STAT- MEDLINE
DCOM- 20100813
LR  - 20131121
IS  - 1095-9157 (Electronic)
IS  - 0896-8411 (Linking)
VI  - 34
IP  - 4
DP  - 2010 Jun
TI  - The role of dendritic cell subsets in 2,4,6-trinitrobenzene sulfonic acid-induced 
      ileitis.
PG  - 380-9
LID - 10.1016/j.jaut.2009.10.002 [doi]
AB  - Dendritic cells (DCs) are widely distributed throughout the lymphoid and 
      nonlymphoid tissues, and are important initiators of acquired immunity and also 
      serve as regulators by inducing self-tolerance. However, it has not been 
      thoroughly clarified whether DCs are involved in the termination of immune 
      responses. In this paper, we have examined the kinetical movement of dendritic 
      cells (DCs) in the lamina propria using the 2,4,6-trinitrobenzene sulfonic acid 
      (TNBS)-induced ileitis model (an animal model for Crohn's disease). Increased 
      numbers of DCs were recruited to the inflammatory sites from day 1 to day 3 at 
      which time the inflammatory responses was clearly observed, then gradually 
      decreased to a steady-state level on day 7 along with the cessation of responses. 
      Three subsets of DCs, PIR-A/B(high), PIR-A/B(med), and PIR-A/B(-) DCs in the 
      CD11c(+)/B220(-) conventional DCs (cDCs) were noted on day 3; the number of 
      PIR-A/B(med) cDCs increased when the inflammatory responses ceased on day 7. The 
      expression of costimulatory molecules such as CD86 and CD54 was lower in the 
      PIR-A/B(med) DCs compared with the other two cDC subsets or splenic DCs. 
      Furthermore, the stimulatory activity of PIR-A/B(med) cDCs was lower than those 
      of PIR-A/B(high) or PIR-A/B(-) cDCs, and far lower than that of splenic DCs. In 
      addition, an increase in the message level of IL-10 was clearly observed in the 
      PIR-A/B(med) cDCs on day 7 while that of proinflammatory cytokines such as IL-6 
      and IL-12 was low. These data demonstrate that PIR-A/B(med) cDCs which increase 
      at the final stage of inflammation may be involved in the termination of the 
      TNBS-induced ileitis by the delivery of anergic signals to effector T cells due 
      to the lower expressions of costimulatory molecules and the production of 
      immunoregulatory cytokine.
FAU - Hoshino, Shoichi
AU  - Hoshino S
AD  - First Department of Pathology, Kansai Medical University, Osaka, Japan.
FAU - Inaba, Muneo
AU  - Inaba M
FAU - Iwai, Hiroshi
AU  - Iwai H
FAU - Ito, Tomoki
AU  - Ito T
FAU - Li, Ming
AU  - Li M
FAU - Gershwin, M Eric
AU  - Gershwin ME
FAU - Okazaki, Kazuichi
AU  - Okazaki K
FAU - Ikehara, Susumu
AU  - Ikehara S
LA  - eng
PT  - Journal Article
DEP - 20091030
PL  - England
TA  - J Autoimmun
JT  - Journal of autoimmunity
JID - 8812164
RN  - 0 (Cytokines)
RN  - 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid)
SB  - IM
MH  - Animals
MH  - Cell Movement/immunology
MH  - Clonal Anergy
MH  - Cytokines/biosynthesis
MH  - Dendritic Cells/*immunology
MH  - Disease Models, Animal
MH  - Ileitis/chemically induced/*immunology/pathology
MH  - Inflammation/immunology
MH  - Mice
MH  - T-Lymphocytes/immunology
MH  - Trinitrobenzenesulfonic Acid/*toxicity
EDAT- 2009/11/03 06:00
MHDA- 2010/08/14 06:00
CRDT- 2009/11/03 06:00
PHST- 2009/08/19 00:00 [received]
PHST- 2009/10/05 00:00 [revised]
PHST- 2009/10/06 00:00 [accepted]
PHST- 2009/11/03 06:00 [entrez]
PHST- 2009/11/03 06:00 [pubmed]
PHST- 2010/08/14 06:00 [medline]
AID - S0896-8411(09)00129-2 [pii]
AID - 10.1016/j.jaut.2009.10.002 [doi]
PST - ppublish
SO  - J Autoimmun. 2010 Jun;34(4):380-9. doi: 10.1016/j.jaut.2009.10.002. Epub 2009 Oct 
      30.