PMID- 27751883
OWN - NLM
STAT- MEDLINE
DCOM- 20170315
LR  - 20240313
IS  - 1879-1166 (Electronic)
IS  - 0198-8859 (Print)
IS  - 0198-8859 (Linking)
VI  - 77
IP  - 12
DP  - 2016 Dec
TI  - FcmuR in human B cell subsets in primary selective IgM deficiency, and regulation 
      of FcmuR and production of natural IgM antibodies by IGIV.
PG  - 1194-1201
LID - S0198-8859(16)30459-1 [pii]
LID - 10.1016/j.humimm.2016.10.003 [doi]
AB  - IgMFcR (FcmuR) are expressed on B cell and B cell subsets. Mice deficient in 
      secreted IgM and FcmuR share properties of impaired specific antibody response and 
      autoimmunity with patient with selective IgM deficiency (SIGMD). Intravenous 
      immunoglobulin (IGIV) regulates immune response, including modulation of IgGFc 
      receptors. However, there are no data on the expression of FcmuR in patients with 
      SIGMD, and the effects of IGIV on FcmuR. In this study, we investigated FcmuR 
      expression in naive marginal zone (MZ), IgM memory, and class-switched memory B 
      cells in patients with selective IgM deficiency and healthy controls. 
      Furthermore, we examined the direct effect of IGIV on FcmuR expression and on the 
      upregulation of FcmuR by TLR2 agonist (Pam3). Finally, we examined the effect of 
      IVIG on spontaneously produced IgM and natural IgM anti-phosphorylcholine (PC) 
      antibodies by B cells and B1 cells. FcmuR expression is significantly decreased in 
      MZ B cells in patients with SIGMD as compared to control. IGIV, at 
      immunomodulatory concentrations, inhibited FcmuR upregulation by Pam3 in MZ B 
      cells, and IgM-depleted IGIV inhibited spontaneous secretion of natural IgM 
      anti-PC antibodies and not total IgM by B1 cells. These data suggest that 
      decreased FcmuR expression on MZ B cells may play a role in the pathogenesis of 
      SIGMD, and an inhibition of TLR-2-induced upregulation of FcmuR by IGIV may be one 
      of the mechanisms of its anti-inflammatory action. IGIV-induced inhibition of 
      natural IgM antibodies may be one of the mechanisms of IGIV-induced 
      immunoregulation.
CI  - Copyright A(c) 2016 American Society for Histocompatibility and Immunogenetics. 
      Published by Elsevier Inc. All rights reserved.
FAU - Gupta, Sudhir
AU  - Gupta S
AD  - Division of Basic and Clinical Immunology, University of California at Irvine, 
      Irvine, CA, USA. Electronic address: sgupta@uci.edu.
FAU - Agrawal, Sudhanshu
AU  - Agrawal S
AD  - Division of Basic and Clinical Immunology, University of California at Irvine, 
      Irvine, CA, USA.
FAU - Gollapudi, Sastry
AU  - Gollapudi S
AD  - Division of Basic and Clinical Immunology, University of California at Irvine, 
      Irvine, CA, USA.
FAU - Kubagawa, Hiromi
AU  - Kubagawa H
AD  - Division of Basic and Clinical Immunology, University of California at Irvine, 
      Irvine, CA, USA.
LA  - eng
GR  - UL1 TR001414/TR/NCATS NIH HHS/United States
PT  - Journal Article
DEP - 20161014
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (Immunoglobulin M)
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Receptors, Fc)
RN  - 0 (immunoglobulin M receptor)
RN  - 0 (secretory IgM)
SB  - IM
MH  - Animals
MH  - Autoimmunity
MH  - B-Lymphocyte Subsets/drug effects/*immunology
MH  - Cells, Cultured
MH  - Humans
MH  - Immunity, Humoral
MH  - Immunoglobulin Class Switching
MH  - Immunoglobulin M/genetics/*metabolism
MH  - Immunoglobulins, Intravenous/therapeutic use
MH  - Immunologic Deficiency Syndromes/*immunology/therapy
MH  - Immunologic Memory
MH  - Immunotherapy/*methods
MH  - Lymphocyte Activation
MH  - Mice
MH  - Receptors, Fc/genetics/*metabolism
PMC - PMC5812685
MID - NIHMS940530
OTO - NOTNLM
OT  - Anti-phosphorylcholine IgM antibodies
OT  - FcmuR
OT  - IGIV
OT  - Marginal zone B cells
OT  - Natural antibodies
OT  - TLR
COIS- CONFLICT OF INTEREST Sudhir Gupta has participated in clinical trials and has 
      served as an ad hoc advisor for Baxalta US, Inc. None of other authors have any 
      conflict of interest.
EDAT- 2016/10/19 06:00
MHDA- 2017/03/16 06:00
PMCR- 2018/02/14
CRDT- 2016/10/19 06:00
PHST- 2016/02/15 00:00 [received]
PHST- 2016/10/11 00:00 [revised]
PHST- 2016/10/12 00:00 [accepted]
PHST- 2016/10/19 06:00 [pubmed]
PHST- 2017/03/16 06:00 [medline]
PHST- 2016/10/19 06:00 [entrez]
PHST- 2018/02/14 00:00 [pmc-release]
AID - S0198-8859(16)30459-1 [pii]
AID - 10.1016/j.humimm.2016.10.003 [doi]
PST - ppublish
SO  - Hum Immunol. 2016 Dec;77(12):1194-1201. doi: 10.1016/j.humimm.2016.10.003. Epub 
      2016 Oct 14.