scholarly journals A Protease-Activated Pathway Underlying Th Cell Type 2 Activation and Allergic Lung Disease

2002 ◽  
Vol 169 (10) ◽  
pp. 5904-5911 ◽  
Author(s):  
Farrah Kheradmand ◽  
Attila Kiss ◽  
Jie Xu ◽  
Seung-Hyo Lee ◽  
Pappachan E. Kolattukudy ◽  
...  
2013 ◽  
Vol 110 (20) ◽  
pp. 8152-8157 ◽  
Author(s):  
Y. Jia ◽  
J. Domenico ◽  
K. Takeda ◽  
J. Han ◽  
M. Wang ◽  
...  

2004 ◽  
Vol 190 (10) ◽  
pp. 1804-1811 ◽  
Author(s):  
Joseph A. Jackson ◽  
Joseph D. Turner ◽  
Lawrence Rentoul ◽  
Helen Faulkner ◽  
Jerzy M. Behnke ◽  
...  

2006 ◽  
Vol 36 (9) ◽  
pp. 1109-1114 ◽  
Author(s):  
N. Hizawa ◽  
M. Kawaguchi ◽  
S.-K. Huang ◽  
M. Nishimura

2020 ◽  
Vol 40 (5) ◽  
pp. 1110-1122 ◽  
Author(s):  
Prasad Srikakulapu ◽  
Coleen A. McNamara

The immune system plays an important role in obesity-induced adipose tissue inflammation and the resultant metabolic dysfunction, which can lead to hypertension, dyslipidemia, and insulin resistance and their downstream sequelae of type 2 diabetes mellitus and cardiovascular disease. While macrophages are the most abundant immune cell type in adipose tissue, other immune cells are also present, such as B cells, which play important roles in regulating adipose tissue inflammation. This brief review will overview B-cell subsets, describe their localization in various adipose depots and summarize our knowledge about the function of these B-cell subsets in regulating adipose tissue inflammation, obesity-induced metabolic dysfunction and atherosclerosis.


1999 ◽  
Vol 190 (7) ◽  
pp. 895-902 ◽  
Author(s):  
Anthony J. Coyle ◽  
Clare Lloyd ◽  
Jane Tian ◽  
Trang Nguyen ◽  
Christina Erikkson ◽  
...  

T1/ST2 is an orphan receptor of unknown function that is expressed on the surface of murine T helper cell type 2 (Th2), but not Th1 effector cells. In vitro blockade of T1/ST2 signaling with an immunoglobulin (Ig) fusion protein suppresses both differentiation to and activation of Th2, but not Th1 effector populations. In a nascent Th2-dominated response, anti-T1/ST2 monoclonal antibody (mAb) inhibited eosinophil infiltration, interleukin 5 secretion, and IgE production. To determine if these effects were mediated by a direct effect on Th2 cells, we next used a murine adoptive transfer model of Th1- and Th2-mediated lung mucosal immune responses. Administration of either T1/ST2 mAb or T1/ST2-Ig abrogated Th2 cytokine production in vivo and the induction of an eosinophilic inflammatory response, but failed to modify Th1-mediated inflammation. Taken together, our data demonstrate an important role of T1/ST2 in Th2-mediated inflammatory responses and suggest that T1/ST2 may prove to be a novel target for the selective suppression of Th2 immune responses.


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