PMID- 35852798
OWN - NLM
STAT- MEDLINE
DCOM- 20221031
LR  - 20230322
IS  - 1398-9995 (Electronic)
IS  - 0105-4538 (Linking)
VI  - 77
IP  - 11
DP  - 2022 Nov
TI  - Regulatory T cells and immunoglobulin E: A new therapeutic link for autoimmunity?
PG  - 3293-3308
LID - 10.1111/all.15449 [doi]
AB  - Autoimmune diseases have a prevalence of approximately 7 to 9% and are classified 
      as either organ-specific diseases, including type I diabetes, multiple sclerosis, 
      inflammatory bowel disease and myasthenia gravis, or systemic diseases, including 
      systemic lupus erythematosus, rheumatoid arthritis and Sjogren's syndrome. While 
      many advancements have been made in understanding of the mechanisms of autoimmune 
      disease, including the nature of self-tolerance and its breakdown, there remain 
      unmet needs in terms of effective and highly targeted treatments. T regulatory 
      cells (Tregs) are key mediators of peripheral tolerance and are implicated in 
      many autoimmune diseases, either as a result of reduced numbers or altered 
      function. Tregs may be broadly divided into those generated in the thymus 
      (tTregs) and those generated in the periphery (pTregs). Tregs target many 
      different immune cell subsets and tissues to suppress excessive inflammation and 
      to support tissue repair and homeostasis: there is a fine balance between Treg 
      cell stability and the plasticity that is required to adjust Tregs' regulatory 
      purposes to particular immune responses. The central role of immunoglobulin E 
      (IgE) in allergic disease is well recognized, and it is becoming increasingly 
      apparent that this immunoglobulin also has a wider role encompassing other 
      diseases including autoimmune disease. Anti-IgE treatment restores the capacity 
      of plasmacytoid dendritic cells (pDCs) impaired by IgE- high-affinity IgE 
      receptor (FcepsilonR1) cross-linking to induce Tregs in vitro in atopic patients. The 
      finding that anti-IgE therapy restores Treg cell homeostasis, and that this 
      mechanism is associated with clinical improvement in asthma and chronic 
      spontaneous urticaria suggests that anti-IgE therapy may also have a potential 
      role in the treatment of autoimmune diseases in which Tregs are involved.
CI  - (c) 2022 The Authors. Allergy published by European Academy of Allergy and Clinical 
      Immunology and John Wiley & Sons Ltd.
FAU - Palomares, Oscar
AU  - Palomares O
AUID- ORCID: 0000-0003-4516-0369
AD  - Complutense University of Madrid, Madrid, Spain.
FAU - Elewaut, Dirk
AU  - Elewaut D
AUID- ORCID: 0000-0002-7468-974X
AD  - Department of Rheumatology, VIB Center for Inflammation Research, Ghent 
      University, Ghent University Hospital, Ghent, Belgium.
FAU - Irving, Peter M
AU  - Irving PM
AUID- ORCID: 0000-0003-0972-8148
AD  - Guy's and St Thomas' Hospital Foundation Trust, London, UK.
AD  - King's College London, London, UK.
FAU - Jaumont, Xavier
AU  - Jaumont X
AUID- ORCID: 0000-0002-4197-1634
AD  - Novartis Pharma AG, Basel, Switzerland.
FAU - Tassinari, Paolo
AU  - Tassinari P
AUID- ORCID: 0000-0003-0205-1795
AD  - Novartis Pharma AG, Basel, Switzerland.
LA  - eng
GR  - MR/T005564/1/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20220727
PL  - Denmark
TA  - Allergy
JT  - Allergy
JID - 7804028
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Humans
MH  - *Autoimmunity
MH  - T-Lymphocytes, Regulatory
MH  - Immunoglobulin E
MH  - *Autoimmune Diseases
MH  - Immune Tolerance
OTO - NOTNLM
OT  - anti-IgE
OT  - autoimmune disease
OT  - immunoglobulin E
OT  - omalizumab
OT  - regulatory T cells
EDAT- 2022/07/20 06:00
MHDA- 2022/11/01 06:00
CRDT- 2022/07/19 11:32
PHST- 2022/07/07 00:00 [revised]
PHST- 2022/01/07 00:00 [received]
PHST- 2022/07/14 00:00 [accepted]
PHST- 2022/07/20 06:00 [pubmed]
PHST- 2022/11/01 06:00 [medline]
PHST- 2022/07/19 11:32 [entrez]
AID - 10.1111/all.15449 [doi]
PST - ppublish
SO  - Allergy. 2022 Nov;77(11):3293-3308. doi: 10.1111/all.15449. Epub 2022 Jul 27.