Lymphocyte-independent connective tissue mast cells populate murine synovium.
Lymphocyte-independent connective tissue mast cells populate murine synovium.
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小鼠滑膜中分布着非淋巴细胞依赖性结缔组织肥大细胞。
DOI:
10.1002/art.22058
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发表时间:
2006
影响因子:
--
通讯作者:
Lee,DavidM
中科院分区:
文献类型:
--
作者:
Shin,Kichul;Gurish,MichaelF;Friend,DanielS;Pemberton,AlanD;Thornton,ElisabethM;Miller,HughR;Lee,DavidM
ObjectiveMast cells (MCs) are a heterogeneous population of tissue‐resident bone marrow–derived cells; distinct MC subpopulations are situated at specific microanatomic locations. The phenotype of the murine synovial MC remains undefined. Since MCs have been implicated in the pathogenesis of inflammatory arthritis, we sought to define the phenotype of the murine synovial MC population in normal and arthritic joints. We also examined the contribution of lymphocytes to synovial MC physiology.MethodsThe MC phenotype in healthy and K/BxN serum transfer–induced arthritic synovial tissue was defined using immunohistochemical staining of prototypic MC‐specific proteases (murine MC proteases [mMCP] 1, 2, 4, 5, 6, and 7) (chymases and tryptases). MC numbers and density were determined by histomorphometry in healthy and arthritic synovia. The lymphocyte contribution to MC populations was assessed using RAG‐null mice.ResultsWe found that synovial MCs display a connective tissue mast cell (CTMC) phenotype in both normal and arthritic synovial tissue, which expresses mMCP‐4, ‐5, ‐6, and ‐7, but not mMCP‐1 or mMCP‐2. In addition, MC hyperplasia was seen in the arthritic synovium. In RAG‐null mice, the phenotype and degree of MC hyperplasia were identical to those observed in normal mice with and without arthritis. Furthermore, in contrast to skin CTMCs, all synovial MCs expressed mMCP‐6, demonstrating discrete differences between synovial CTMCs and other anatomic CTMC populations.ConclusionOur findings demonstrate that the murine synovial MC population is composed of lymphocyte‐independent CTMCs and identify arthritic synovium as a model system by which to gain insight into the poorly understood physiology of CTMCs in chronic inflammation.
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DOI:
10.1084/jem.160.1.12
发表时间:
1984-07-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Guy-Grand D;Dy M;Luffau G;Vassalli P
通讯作者:
Vassalli P
影响因子:
15.9
作者:
Blair, RJ;Meng, H;Gruber, BL
通讯作者:
Gruber, BL
影响因子:
4.4
作者:
A. Irani;S. Craig;G. Deblois;C. Elson;N. Schechter;L. Schwartz
通讯作者:
A. Irani;S. Craig;G. Deblois;C. Elson;N. Schechter;L. Schwartz
影响因子:
15.3
作者:
OTSU, K;NAKANO, T;KANAKURA, Y;ASAI, H;KATZ, HR;AUSTEN, KF;STEVENS, RL;GALLI, SJ;KITAMURA, Y
通讯作者:
KITAMURA, Y
DOI:
--
发表时间:
1992
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
McNeil,HP;Frenkel,DP;Austen,KF;Friend,DS;Stevens,RL
通讯作者:
Stevens,RL