PMID- 27981054
OWN - NLM
STAT- MEDLINE
DCOM- 20170320
LR  - 20181113
IS  - 2314-7156 (Electronic)
IS  - 2314-8861 (Print)
IS  - 2314-7156 (Linking)
VI  - 2016
DP  - 2016
TI  - Complement Receptor Type 1 Suppresses Human B Cell Functions in SLE Patients.
PG  - 5758192
LID - 5758192
AB  - Complement receptors (CRs) play an integral role in innate immunity and also 
      function to initiate and shape the adaptive immune response. Our earlier results 
      showed that complement receptor type 1 (CR1, CD35) is a potent inhibitor of the B 
      cell receptor- (BCR-) induced functions of human B lymphocytes. Here we show that 
      this inhibition occurs already at the initial steps of B cell activation since 
      ligation of CR1 reduces the BCR-induced phosphorylation of key signaling 
      molecules such as Syk and mitogen activated protein kinases (MAPKs). Furthermore, 
      our data give evidence that although B lymphocytes of active systemic lupus 
      erythematosus (SLE) patients express lower level of CR1, the inhibitory capacity 
      of this complement receptor is still maintained and its ligand-induced clustering 
      results in significant inhibition of the main B cell functions, similar to that 
      found in the case of healthy individuals. Since we have found that reduced CR1 
      expression of SLE patients does not affect the inhibitory capacity of the 
      receptor, our results further support the therapeutical potential of CD35 
      targeting the decrease of B cell activation and autoantibody production in 
      autoimmune patients.
FAU - Kremlitzka, Mariann
AU  - Kremlitzka M
AD  - MTA-ELTE Immunology Research Group, Budapest, Eotvos Lorand University, Pazmany 
      Peter s. 1/C, Budapest 1117, Hungary.
FAU - Macsik-Valent, Bernadett
AU  - Macsik-Valent B
AD  - Department of Immunology, Eotvos Lorand University, Pazmany Peter s. 1/C, 
      Budapest 1117, Hungary.
FAU - Polgar, Anna
AU  - Polgar A
AD  - Institute of Rheumatology and Physiotherapy, Frankel Leo u. 25-29, Budapest 1023, 
      Hungary.
FAU - Kiss, Emese
AU  - Kiss E
AUID- ORCID: 0000-0002-5399-2379
AD  - Institute of Rheumatology and Physiotherapy, Frankel Leo u. 25-29, Budapest 1023, 
      Hungary.
FAU - Poor, Gyula
AU  - Poor G
AD  - Institute of Rheumatology and Physiotherapy, Frankel Leo u. 25-29, Budapest 1023, 
      Hungary.
FAU - Erdei, Anna
AU  - Erdei A
AUID- ORCID: 0000-0002-3622-6680
AD  - MTA-ELTE Immunology Research Group, Budapest, Eotvos Lorand University, Pazmany 
      Peter s. 1/C, Budapest 1117, Hungary; Department of Immunology, Eotvos Lorand 
      University, Pazmany Peter s. 1/C, Budapest 1117, Hungary.
LA  - eng
PT  - Journal Article
DEP - 20161117
PL  - Egypt
TA  - J Immunol Res
JT  - Journal of immunology research
JID - 101627166
RN  - 0 (Autoantibodies)
RN  - 0 (CR1 protein, human)
RN  - 0 (Receptors, Antigen, B-Cell)
RN  - 0 (Receptors, Complement 3b)
RN  - EC 2.7.10.2 (SYK protein, human)
RN  - EC 2.7.10.2 (Syk Kinase)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Adult
MH  - Autoantibodies/immunology
MH  - B-Lymphocytes/*immunology/physiology
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Female
MH  - Flow Cytometry
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*immunology
MH  - Lymphocyte Activation
MH  - Male
MH  - Middle Aged
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Phosphorylation
MH  - Receptors, Antigen, B-Cell/immunology
MH  - Receptors, Complement 3b/*immunology/*metabolism
MH  - Syk Kinase/metabolism
PMC - PMC5131247
COIS- The authors declare no financial or commercial conflict of interests.
EDAT- 2016/12/17 06:00
MHDA- 2017/03/21 06:00
PMCR- 2016/11/17
CRDT- 2016/12/17 06:00
PHST- 2016/08/03 00:00 [received]
PHST- 2016/10/18 00:00 [accepted]
PHST- 2016/12/17 06:00 [entrez]
PHST- 2016/12/17 06:00 [pubmed]
PHST- 2017/03/21 06:00 [medline]
PHST- 2016/11/17 00:00 [pmc-release]
AID - 10.1155/2016/5758192 [doi]
PST - ppublish
SO  - J Immunol Res. 2016;2016:5758192. doi: 10.1155/2016/5758192. Epub 2016 Nov 17.