PMID- 30121255
OWN - NLM
STAT- MEDLINE
DCOM- 20190830
LR  - 20190830
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 188
IP  - 11
DP  - 2018 Nov
TI  - Helminth Antigen-Conditioned Dendritic Cells Generate Anti-Inflammatory Cd4 T 
      Cells Independent of Antigen Presentation via Major Histocompatibility Complex 
      Class II.
PG  - 2589-2604
LID - S0002-9440(17)31172-0 [pii]
LID - 10.1016/j.ajpath.2018.07.008 [doi]
AB  - A recently identified feature of the host response to infection with helminth 
      parasites is suppression of concomitant disease. Dendritic cells (DCs) exposed to 
      antigens from the tapeworm Hymenolepis diminuta significantly reduce the severity 
      of dinitrobenzene sulfonic acid-induced colitis in mice. Here we elucidate 
      mechanisms underlying this cellular immunotherapy. We show a requirement for Ccr7 
      expression on transferred H. diminuta antigen-treated (HD)-DCs, suggesting that 
      homing to secondary lymphoid tissues is important for suppression of colitis. 
      Furthermore, sodium metaperiodate-sensitive helminth-derived glycans are required 
      to drive the anti-colitic response in recipient mice. Induction of Th2-type 
      cytokines and Gata-3(+)Cd4(+) cells in secondary lymphoid tissues is dependent on 
      major histocompatibility complex class II (MHC II) protein expression on 
      transferred DCs, although remarkably, transfer of MHC II(-/-) HD-DCs still 
      attenuated dinitrobenzene sulfonic acid-induced colitis in recipient mice. 
      Moreover, transfer of Cd4(+) splenic T cells retrieved from mice administered MHC 
      II(-/-) HD-DCs suppressed dinitrobenzene sulfonic acid-induced colitis in 
      recipient mice. Our studies reveal that HD-DCs can suppress colitis via an 
      alternative MHC II-independent pathway that involves, in part, mobilization of 
      T-cell responses. These data support the utility of HD-DCs in blocking colitis, 
      revealing a requirement for Ccr7 and providing for HD-DC autologous immunotherapy 
      for disease in which MHC II expression and/or function is compromised.
CI  - Copyright (c) 2018 American Society for Investigative Pathology. Published by 
      Elsevier Inc. All rights reserved.
FAU - Matisz, Chelsea E
AU  - Matisz CE
AD  - Gastrointestinal Research Group and Inflammation Research Network, Department of 
      Physiology and Pharmacology, Snyder Institute for Chronic Diseases, Cumming 
      School of Medicine, University of Calgary, Calgary, Alberta, Canada.
FAU - Geuking, Markus B
AU  - Geuking MB
AD  - Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute 
      for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, 
      Alberta, Canada.
FAU - Lopes, Fernando
AU  - Lopes F
AD  - Gastrointestinal Research Group and Inflammation Research Network, Department of 
      Physiology and Pharmacology, Snyder Institute for Chronic Diseases, Cumming 
      School of Medicine, University of Calgary, Calgary, Alberta, Canada.
FAU - Petri, Bjorn
AU  - Petri B
AD  - Mouse Phenomics Resource Laboratory, Department of Microbiology, Immunology and 
      Infectious Diseases, Snyder Institute for Chronic Diseases, Cumming School of 
      Medicine, University of Calgary, Calgary, Alberta, Canada.
FAU - Wang, Arthur
AU  - Wang A
AD  - Gastrointestinal Research Group and Inflammation Research Network, Department of 
      Physiology and Pharmacology, Snyder Institute for Chronic Diseases, Cumming 
      School of Medicine, University of Calgary, Calgary, Alberta, Canada.
FAU - Sharkey, Keith A
AU  - Sharkey KA
AD  - Gastrointestinal Research Group and Inflammation Research Network, Department of 
      Physiology and Pharmacology, Snyder Institute for Chronic Diseases, Cumming 
      School of Medicine, University of Calgary, Calgary, Alberta, Canada; Hotchkiss 
      Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, 
      Alberta, Canada.
FAU - McKay, Derek M
AU  - McKay DM
AD  - Gastrointestinal Research Group and Inflammation Research Network, Department of 
      Physiology and Pharmacology, Snyder Institute for Chronic Diseases, Cumming 
      School of Medicine, University of Calgary, Calgary, Alberta, Canada. Electronic 
      address: dmckay@ucalgary.ca.
LA  - eng
GR  - PJT 391060/CIHR/Canadian Institutes of Health Research/Canada
GR  - FDN 148380/CIHR/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180817
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antigens, Helminth)
RN  - 0 (Cytokines)
RN  - 0 (Histocompatibility Antigens Class II)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Antigen Presentation/*immunology
MH  - Antigens, Helminth/*immunology
MH  - CD4-Positive T-Lymphocytes/*immunology
MH  - Colitis/chemically induced/immunology/*prevention & control
MH  - Cytokines
MH  - Dendritic Cells/*immunology
MH  - Histocompatibility Antigens Class II/*physiology
MH  - Hymenolepis diminuta/immunology
MH  - Immunotherapy
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
EDAT- 2018/08/20 06:00
MHDA- 2019/08/31 06:00
CRDT- 2018/08/20 06:00
PHST- 2017/12/10 00:00 [received]
PHST- 2018/07/09 00:00 [revised]
PHST- 2018/07/16 00:00 [accepted]
PHST- 2018/08/20 06:00 [pubmed]
PHST- 2019/08/31 06:00 [medline]
PHST- 2018/08/20 06:00 [entrez]
AID - S0002-9440(17)31172-0 [pii]
AID - 10.1016/j.ajpath.2018.07.008 [doi]
PST - ppublish
SO  - Am J Pathol. 2018 Nov;188(11):2589-2604. doi: 10.1016/j.ajpath.2018.07.008. Epub 
      2018 Aug 17.