PMID- 33139384
OWN - NLM
STAT- MEDLINE
DCOM- 20210726
LR  - 20210726
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Print)
IS  - 0019-9567 (Linking)
VI  - 89
IP  - 2
DP  - 2021 Jan 19
TI  - Adoptive Transfer of Group 3-Like Innate Lymphoid Cells Restores Mouse Colon 
      Resistance to Colonization of a Gamma Interferon-Susceptible Chlamydia muridarum 
      Mutant.
LID - 10.1128/IAI.00533-20 [doi]
LID - e00533-20
AB  - The obligate intracellular bacterium Chlamydia muridarum can colonize the mouse 
      colon for a long period, but a gamma interferon (IFN-gamma)-susceptible mutant clone 
      fails to do so. Nevertheless, the mutant's colonization is rescued in mice 
      deficient in interleukin-7 receptor (IL-7R) (lacking both lymphocytes and innate 
      lymphoid cells [ILCs]) or IFN-gamma but not in mice lacking recombination-activated 
      gene 1 (Rag1(-/-) mice) (lacking adaptive immunity lymphocytes), indicating a 
      critical role of ILC-derived IFN-gamma in regulating chlamydial colonization. In the 
      current study, we have used an adoptive transfer approach for further 
      characterizing the responsible ILCs. First, intestinal ILCs isolated from 
      Rag1(-/-) mice were able to rescue IL-7R-deficient mice to restrict the 
      colonization of the IFN-gamma-susceptible Chlamydia muridarum mutant. Second, the 
      responsible ILCs were localized to the intestinal lamina propria since ILCs from 
      the lamina propria but not the intraepithelial compartment conferred the 
      restriction. Third, lamina propria ILCs enriched for RORgammat expression but not 
      those negative for RORgammat rescued the IL-7R-deficient mice to restrict mutant 
      colonization, indicating a critical role of group 3-like ILCs (ILC3s) since RORgammat 
      is a signature transcriptional factor of ILC3s. Fourth, a portion of the ILC3s 
      expressed IFN-gamma, thus defined as ex-ILC3s, and the transfer of the ex-ILC3s 
      conferred colon resistance to mutant Chlamydia muridarum colonization in 
      IFN-gamma-deficient mice. Finally, genetically labeled RORgammat-positive (RORgammat(+)) ILCs 
      were able to inhibit mutant colonization. Thus, we have demonstrated that ILC3s 
      are sufficient for regulating chlamydial colonization, laying a foundation for 
      further revealing the mechanisms by which an obligate intracellular bacterium 
      activates colonic ILC3s.
CI  - Copyright (c) 2021 American Society for Microbiology.
FAU - He, Ying
AU  - He Y
AD  - Department of Microbiology, Immunology and Molecular Genetics, University of 
      Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
AD  - Department of Gastroenterology, Xiangya Hospital, Central South University, 
      Changsha, Hunan, China.
FAU - Xu, Hong
AU  - Xu H
AD  - Department of Microbiology, Immunology and Molecular Genetics, University of 
      Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
FAU - Song, Chenchen
AU  - Song C
AD  - Department of Microbiology, Immunology and Molecular Genetics, University of 
      Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
FAU - Koprivsek, John J
AU  - Koprivsek JJ
AD  - Department of Microbiology, Immunology and Molecular Genetics, University of 
      Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
FAU - Arulanandam, Bernard
AU  - Arulanandam B
AD  - Department of Biology, University of Texas at San Antonio, San Antonio, Texas, 
      USA.
FAU - Yang, Huixiang
AU  - Yang H
AD  - Department of Gastroenterology, Xiangya Hospital, Central South University, 
      Changsha, Hunan, China.
FAU - Tao, Lijian
AU  - Tao L
AD  - Department of Nephrology, Xiangya Hospital, Central South University, Changsha, 
      Hunan, China.
FAU - Zhong, Guangming
AU  - Zhong G
AUID- ORCID: 0000-0001-7053-5009
AD  - Department of Microbiology, Immunology and Molecular Genetics, University of 
      Texas Health Science Center at San Antonio, San Antonio, Texas, USA 
      Zhongg@UTHSCSA.edu.
LA  - eng
GR  - R01 AI047997/AI/NIAID NIH HHS/United States
GR  - R01 AI121989/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20210119
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Chlamydia Infections/*therapy
MH  - Chlamydia muridarum/*genetics/*immunology/*pathogenicity
MH  - Colon/microbiology
MH  - Disease Models, Animal
MH  - Disease Resistance/genetics/*immunology
MH  - Genetic Variation
MH  - Genotype
MH  - Humans
MH  - Immunity, Innate/*genetics
MH  - Interferon-gamma/immunology
MH  - Lymphocyte Transfusion
MH  - Lymphocytes/*immunology
MH  - Mice
MH  - Mutation
MH  - Virulence/genetics/immunology
PMC - PMC7822149
OTO - NOTNLM
OT  - Chlamydia
OT  - IFN-gamma
OT  - adoptive transfer
OT  - colon
OT  - ex-ILC3s
OT  - innate lymphoid cells
OT  - spreading
EDAT- 2020/11/04 06:00
MHDA- 2021/07/27 06:00
PMCR- 2021/07/19
CRDT- 2020/11/03 05:38
PHST- 2020/08/22 00:00 [received]
PHST- 2020/10/29 00:00 [accepted]
PHST- 2020/11/04 06:00 [pubmed]
PHST- 2021/07/27 06:00 [medline]
PHST- 2020/11/03 05:38 [entrez]
PHST- 2021/07/19 00:00 [pmc-release]
AID - IAI.00533-20 [pii]
AID - 00533-20 [pii]
AID - 10.1128/IAI.00533-20 [doi]
PST - epublish
SO  - Infect Immun. 2021 Jan 19;89(2):e00533-20. doi: 10.1128/IAI.00533-20. Print 2021 
      Jan 19.