PMID- 28790503
OWN - NLM
STAT- MEDLINE
DCOM- 20180514
LR  - 20181113
IS  - 0065-7778 (Print)
IS  - 0065-7778 (Linking)
VI  - 128
DP  - 2017
TI  - Mast Cells and IgE can Enhance Survival During Innate and Acquired Host Responses 
      to Venoms.
PG  - 193-221
AB  - Mast cells and immunoglobulin E (IgE) antibodies are thought to promote health by 
      contributing to host responses to certain parasites, but other beneficial 
      functions have remained obscure. Venoms provoke innate inflammatory responses and 
      pathology reflecting the activities of the contained toxins. Venoms also can 
      induce allergic sensitization and development of venom-specific IgE antibodies, 
      which can predispose some subjects to exhibit anaphylaxis upon subsequent 
      exposure to the relevant venom. We found that innate functions of mast cells, 
      including degradation of venom toxins by mast cell-derived proteases, enhanced 
      survival in mice injected with venoms from the honeybee, two species of scorpion, 
      three species of poisonous snakes, or the Gila monster. We also found that mice 
      injected with sub-lethal amounts of honeybee or Russell's viper venom exhibited 
      enhanced survival after subsequent challenge with potentially lethal amounts of 
      that venom, and that IgE antibodies, FcepsilonRI, and probably mast cells contributed 
      to such acquired resistance.
FAU - Galli, Stephen J
AU  - Galli SJ
AD  - STANFORD, CALIFORNIA.
FAU - Starkl, Philipp
AU  - Starkl P
AD  - STANFORD, CALIFORNIA.
FAU - Marichal, Thomas
AU  - Marichal T
AD  - STANFORD, CALIFORNIA.
FAU - Tsai, Mindy
AU  - Tsai M
AD  - STANFORD, CALIFORNIA.
LA  - eng
GR  - R01 AR067145/AR/NIAMS NIH HHS/United States
GR  - R01 CA072074/CA/NCI NIH HHS/United States
GR  - R37 AI023990/AI/NIAID NIH HHS/United States
GR  - U19 AI104209/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Trans Am Clin Climatol Assoc
JT  - Transactions of the American Clinical and Climatological Association
JID - 7507559
RN  - 0 (Antibodies)
RN  - 0 (Venoms)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Adaptive Immunity/*physiology
MH  - Animals
MH  - Antibodies/immunology
MH  - Immunity, Innate/*physiology
MH  - Immunoglobulin E/*physiology
MH  - Mast Cells/*physiology
MH  - Venoms/*toxicity
PMC - PMC5525434
COIS- Potential Conflicts of Interest: The work reviewed herein was supported by grants 
      to Dr. Galli from the National Institutes of Health (e.g., R37 AI23990, R01 
      CA072074, R01 AR067145, and U19 AI104209) and the National Science Foundation, 
      and from several other funding sources, including the Department of Pathology at 
      Stanford University. Dr. Starkl was supported by a Max Kade Fellowship of the Max 
      Kade Foundation and the Austrian Academy of Sciences, a Schroedinger Fellowship 
      of the Austrian Science Fund (FWF): J3399-B21, and a Marie Curie fellowship of 
      the European Commission (H2020-MSCA-IF-2014), 655153. Dr. Marichal was supported 
      by a Marie Curie International Outgoing Fellowship for Career Development: 
      European Union's Seventh Framework Programme (FP7-PEOPLE-2011-IOF), 299954, and a 
      "Charge de recherches" fellowship of the Belgian National Fund for Scientific 
      Research (F.R.S-FNRS).
EDAT- 2017/08/10 06:00
MHDA- 2018/05/15 06:00
PMCR- 2017/01/01
CRDT- 2017/08/10 06:00
PHST- 2017/08/10 06:00 [entrez]
PHST- 2017/08/10 06:00 [pubmed]
PHST- 2018/05/15 06:00 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
PST - ppublish
SO  - Trans Am Clin Climatol Assoc. 2017;128:193-221.