PMID- 19651179
OWN - NLM
STAT- MEDLINE
DCOM- 20100129
LR  - 20171116
IS  - 1879-1166 (Electronic)
IS  - 0198-8859 (Linking)
VI  - 70
IP  - 12
DP  - 2009 Dec
TI  - Potential role of soluble human leukocyte antigen-G molecules in multiple 
      sclerosis.
PG  - 981-7
LID - 10.1016/j.humimm.2009.07.014 [doi]
AB  - Nonclassical human leukocyte antigen (HLA)-G antigens in soluble form (sHLA-G) 
      have recently been suggested to have a potential role as immunomodulatory factors 
      in multiple sclerosis (MS), a chronic inflammatory demyelinating and 
      neurodegenerative disease of the central nervous system of unknown etiology and 
      supposed autoimmune origin. In MS patients, sHLA-G levels were elevated in 
      cerebrospinal fluid (CSF), intrathecally synthesized, predominantly represented 
      by the HLA-G5 isoform and even more elevated in cases of inactive disease, as 
      determined by magnetic resonance imaging. In MS, CSF sHLA-G concentrations were 
      also related to the formation of an intrathecal anti-inflammatory 
      microenvironment based on a positive correlation to CSF interleukin-10 titers and 
      an inverse association to the levels of antiapoptotic sFas molecules in the CSF. 
      Expression of HLA-G antigens was detected in microglia, macrophages, and 
      endothelial cells within and around MS lesions and was enhanced in microglial 
      cells by T-helper-1 proinflammatory cytokines. A novel subpopulation of naturally 
      occurring CD4(+) and CD8(+) regulatory T cells expressing HLA-G1 and secreting 
      HLA-G5 was identified in the CSF of MS patients. Taken together, these findings 
      seem to indicate that sHLA-G antigens may be implicated in the termination of MS 
      autoimmunity and associated with remission of the disease through their function 
      as anti-inflammatory molecules. However, the mechanisms operating in the 
      immunomodulatory circuit mediated by sHLA-G proteins remain to be clarified.
FAU - Fainardi, Enrico
AU  - Fainardi E
AD  - Department of Neurosciences and Rehabilitation, Azienda 
      Ospedaliera-Universitaria, Arcispedale S Anna, Ferrara, Italy. henryfai@tin.it
FAU - Rizzo, Roberta
AU  - Rizzo R
FAU - Castellazzi, Massimiliano
AU  - Castellazzi M
FAU - Stignani, Marina
AU  - Stignani M
FAU - Granieri, Enrico
AU  - Granieri E
FAU - Baricordi, Olavio Roberto
AU  - Baricordi OR
LA  - eng
PT  - Journal Article
DEP - 20090806
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-G Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (fas Receptor)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Autoimmunity/immunology
MH  - HLA Antigens/cerebrospinal fluid/*immunology
MH  - HLA-G Antigens
MH  - Histocompatibility Antigens Class I/cerebrospinal fluid/*immunology
MH  - Humans
MH  - Interleukin-10/cerebrospinal fluid
MH  - Multiple Sclerosis/*immunology/physiopathology
MH  - T-Lymphocyte Subsets/*immunology
MH  - fas Receptor/cerebrospinal fluid
EDAT- 2009/08/05 09:00
MHDA- 2010/01/30 06:00
CRDT- 2009/08/05 09:00
PHST- 2009/05/29 00:00 [received]
PHST- 2009/07/24 00:00 [revised]
PHST- 2009/07/28 00:00 [accepted]
PHST- 2009/08/05 09:00 [entrez]
PHST- 2009/08/05 09:00 [pubmed]
PHST- 2010/01/30 06:00 [medline]
AID - S0198-8859(09)00189-X [pii]
AID - 10.1016/j.humimm.2009.07.014 [doi]
PST - ppublish
SO  - Hum Immunol. 2009 Dec;70(12):981-7. doi: 10.1016/j.humimm.2009.07.014. Epub 2009 
      Aug 6.