PMID- 28747348
DCOM- 20170929
LR  - 20181113
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 199
IP  - 5
DP  - 2017 Sep 1
TI  - Lactation-Based Maternal Educational Immunity Crosses MHC Class I Barriers and
      Can Impart Th1 Immunity to Th2-Biased Recipients.
PG  - 1729-1736
LID - 10.4049/jimmunol.1601375 [doi]
AB  - We have previously demonstrated lactational transfer of T cell-based immunity
      from dam to foster pup. In the short term, a significant part of transferred
      immunity is passive cellular immunity. However, as time progresses, this is
      replaced by what we have described as maternal educational immunity such that by 
      young adulthood, all immune cells responding to a foster dam immunogen are the
      product of the foster pup's thymus. To reduce confounding factors, this original 
      demonstration used congenic/syngeneic dam and foster pup pairs. In this study, we
      investigated lactational transfer of immunity to Mycobacterium tuberculosis in
      MHC class I-mismatched animals, as well as from Th1-biased dams to Th2-biased
      foster pups. Using immunized C57BL/6J dams, lactational transfer to nonimmunized 
      BALB/cJ foster pups resulted in much greater immunity than direct immunization in
      5-wk-old pups (ex vivo assay of pup splenocytes). At this age, 82% of
      immunogen-responding cells in the pup spleen were produced through maternal
      educational immunity. FVB/NJ nonimmunized foster recipients had a greater number 
      of maternal cells in the spleen and thymus but a much larger percentage was
      Foxp3(+), resulting in equivalent immunity to direct immunization. Depletion of
      maternal Foxp3(+) cells from pup splenocytes illustrated a substantial role for
      lactationally transferred dam regulatory T cells in suppression of the ex vivo
      response in FVB/NJ, but not BALB/cJ, recipients. We conclude that lactational
      transfer of immunity can cross MHC class I barriers and that Th1 immunity can be 
      imparted to Th2-biased offspring; in some instances, it can be greater than that 
      achieved by direct immunization.
CI  - Copyright (c) 2017 by The American Association of Immunologists, Inc.
FAU - Ghosh, Mrinal K
AU  - Ghosh MK
AD  - Division of Biomedical Sciences, School of Medicine, University of California,
      Riverside, Riverside, CA 92521; and.
FAU - Muller, H Konrad
AU  - Muller HK
AD  - School of Medicine, University of Tasmania, Hobart 7000, Tasmania, Australia.
FAU - Walker, Ameae M
AU  - Walker AM
AD  - Division of Biomedical Sciences, School of Medicine, University of California,
      Riverside, Riverside, CA 92521; and
LA  - eng
GR  - HHSN272201300006C/AI/NIAID NIH HHS/United States
GR  - R01 HD065099/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20170726
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Foxp3 protein, mouse)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Isoantigens)
SB  - IM
MH  - Animals
MH  - Female
MH  - Forkhead Transcription Factors/metabolism
MH  - Histocompatibility Antigens Class I/immunology
MH  - *Immunity, Maternally-Acquired
MH  - Isoantigens/immunology
MH  - Lactation/*immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mycobacterium tuberculosis/*immunology
MH  - Pregnancy
MH  - T-Lymphocytes, Regulatory/*immunology
MH  - Th1 Cells/*immunology
MH  - Th1-Th2 Balance
MH  - Th2 Cells/*immunology
MH  - Thymocytes/*immunology
MH  - Tuberculosis/*immunology
PMC - PMC5563164
EDAT- 2017/07/28 06:00
MHDA- 2017/09/30 06:00
CRDT- 2017/07/28 06:00
PHST- 2016/08/08 00:00 [received]
PHST- 2017/06/23 00:00 [accepted]
PHST- 2017/07/28 06:00 [pubmed]
PHST- 2017/09/30 06:00 [medline]
PHST- 2017/07/28 06:00 [entrez]
AID - jimmunol.1601375 [pii]
AID - 10.4049/jimmunol.1601375 [doi]
PST - ppublish
SO  - J Immunol. 2017 Sep 1;199(5):1729-1736. doi: 10.4049/jimmunol.1601375. Epub 2017 
      Jul 26.