Identification of myeloid-derived suppressor cells in the synovial fluid of patients with rheumatoid arthritis: a pilot study.
Identification of myeloid-derived suppressor cells in the synovial fluid of patients with rheumatoid arthritis: a pilot study.
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DOI:
10.1186/1471-2474-15-281
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发表时间:
2014-08-19
影响因子:
2.3
通讯作者:
Mikecz K
中科院分区:
文献类型:
--
作者:
Kurkó J;Vida A;Glant TT;Scanzello CR;Katz RS;Nair A;Szekanecz Z;Mikecz K
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of innate immune cells with a granulocyte-like or monocyte-like phenotype and a unique ability to suppress T-cell responses. MDSCs have been shown to accumulate in cancer patients, but recent studies suggest that these cells are also present in humans and animals suffering from autoimmune diseases. We previously identified MDSCs in the synovial fluid (SF) of mice with experimental autoimmune arthritis. The goal of the present study was to identify MDSCs in the SF of patients with rheumatoid arthritis (RA). RA SF cells were studied by flow cytometry using antibodies to MDSC cell surface markers as well as by analysis of cell morphology. The suppressor activity of RA SF cells toward autologous peripheral blood T cells was determined ex vivo. We employed both antigen-nonspecific (anti-CD3/CD28 antibodies) and antigen-specific (allogeneic cells) induction systems to test the effects of RA SF cells on the proliferation of autologous T cells. SF from RA patients contained MDSC-like cells, the majority of which showed granulocyte (neutrophil)-like phenotype and morphology. RA SF cells significantly suppressed the proliferation of anti-CD3/CD28-stimulated autologous T cells upon co-culture. When compared side by side, RA SF cells had a more profound inhibitory effect on the alloantigen-induced than the anti-CD3/CD28-induced proliferation of autologous T cells. MDSCs are present among RA SF cells that are commonly regarded as inflammatory neutrophils. Our results suggest that the presence of neutrophil-like MDSCs in the SF is likely beneficial, as these cells have the ability to limit the expansion of joint-infiltrating T cells in RA. The online version of this article (doi:10.1186/1471-2474-15-281) contains supplementary material, which is available to authorized users.
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影响因子:
5.6
作者:
Greten TF;Manns MP;Korangy F
通讯作者:
Korangy F
DOI:
10.4049/jimmunol.1000901
发表时间:
2010-08-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Lechner MG;Liebertz DJ;Epstein AL
通讯作者:
Epstein AL
影响因子:
82.9
作者:
Nagaraj, Srinivas;Gupta, Kapil;Gabrilovich, Dmitry I.
通讯作者:
Gabrilovich, Dmitry I.
影响因子:
15.9
作者:
Pillay, Janesh;Kamp, Vera M.;Koenderman, Leo
通讯作者:
Koenderman, Leo
DOI:
10.1186/ar557
发表时间:
2002
期刊:
Arthritis research
影响因子:
--
作者:
Cope AP
通讯作者:
Cope AP