scholarly journals Interleukin 4 increases human synovial cell expression of VCAM-1 and T cell binding.

1994 ◽  
Vol 53 (9) ◽  
pp. 601-607 ◽  
Author(s):  
H Shimada ◽  
K Eguchi ◽  
Y Ueki ◽  
M Nakashima ◽  
I Yamashita ◽  
...  
Immunology ◽  
2007 ◽  
Vol 120 (1) ◽  
Author(s):  
Suranjith L. Seneviratne ◽  
Antony P. Black ◽  
Louise Jones ◽  
Kati di Gleria ◽  
Abigail S. Bailey ◽  
...  

2009 ◽  
Vol 2009 ◽  
pp. 1-4 ◽  
Author(s):  
F. Mori ◽  
S. Barni ◽  
A. Cianferoni ◽  
N. Pucci ◽  
M. de Martino ◽  
...  

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated food allergy characterized by severe vomiting, diarrhea, and often failure to thrive in infants. Symptoms typically resolve after the triggering food-derived protein is removed from the diet and recur within few hours after the re-exposure to the causal protein. The diagnosis is based on clinical symptoms and a positive food challenge. In this study, we report a case of FPIES to rice in an 8-month-old boy. We performed a double-blind placebo-controlled food challenge (DBPCFC) to rice and we measured the intracellular T cell expression of interleukin-4 (IL-4); IL-10, and interferon (IFN-) pre-and post-challenge during an acute FPIES reaction and when tolerance to rice had been achieved. For the first time we describe an increase in T cell IL-4 and decrease in IFN- expression after a positive challenge with rice (i.e. rice triggered a FPIES attack) and an increase in T cell IL-10 expression after rice challenge 6 months later after a negative challenge (i.e., the child had acquired tolerance to rice) in an 8 month old with documented FPIES to rice. A Th2 activation associated with high IL-4 levels may contribute to the pathophysiology of the disease. On the other hand, T cell-derived IL-10 may play a role in the acquisition of immunotolerance by regulating the Th1 and Th2 responses.


1999 ◽  
Vol 190 (5) ◽  
pp. 607-616 ◽  
Author(s):  
Hideki Iijima ◽  
Ichiro Takahashi ◽  
Daisuke Kishi ◽  
Jin-Kyung Kim ◽  
Sunao Kawano ◽  
...  

T cell receptor α chain–deficient (TCR-α−/−) mice are known to spontaneously develop inflammatory bowel disease (IBD). The colitis that develops in these mice is associated with increased numbers of T helper cell (Th)2-type CD4+TCR-ββ (CD4+ββ) T cells producing predominantly interleukin (IL)-4. To investigate the role of these Th2-type CD4+ββ T cells, we treated TCR-α−/− mice with anti–IL-4 monoclonal antibody (mAb). Approximately 60% of TCR-α−/− mice, including those treated with mock Ab and those left untreated, spontaneously developed IBD. However, anti–IL-4 mAb–treated mice exhibited no clinical or histological signs of IBD, and their levels of mucosal and systemic Ab responses were lower than those of mock Ab–treated mice. Although TCR-α−/− mice treated with either specific or mock Ab developed CD4+ββ T cells, only those treated with anti–IL-4 mAb showed a decrease in Th2-type cytokine production at the level of mRNA and protein and an increase in interferon γ–specific expression. These findings suggest that IL-4–producing Th2-type CD4+ββ T cells play a major immunopathological role in the induction of IBD in TCR-α−/− mice, a role that anti–IL-4 mAb inhibits by causing Th2-type CD4+ββ T cells to shift to the Th1 type.


1999 ◽  
Vol 274 (10) ◽  
pp. 6567-6578 ◽  
Author(s):  
Jean-Marc Grégoire ◽  
Paul-Henri Roméo
Keyword(s):  
T Cell ◽  

1989 ◽  
Vol 27 (3-4) ◽  
pp. 448-450 ◽  
Author(s):  
M. L. Watson ◽  
G. P. Lewis ◽  
J. Westwick

2013 ◽  
Vol 191 (8) ◽  
pp. 4269-4279 ◽  
Author(s):  
Lauren C. Frazer ◽  
Jeanne E. Sullivan ◽  
Matthew A. Zurenski ◽  
Margaret Mintus ◽  
Tammy E. Tomasak ◽  
...  

2009 ◽  
Vol 52 (3) ◽  
pp. 191-192 ◽  
Author(s):  
N. Mori ◽  
F. Shirakawa ◽  
S. Murakami ◽  
S. Oda ◽  
S. Eto

Blood ◽  
1993 ◽  
Vol 81 (5) ◽  
pp. 1352-1358 ◽  
Author(s):  
G Migliorati ◽  
I Nicoletti ◽  
MC Pagliacci ◽  
L D'Adamio ◽  
C Riccardi

Abstract Glucocorticoid hormones (GCH) and anti-CD3 monoclonal antibodies (MoAbs) induce in mouse thymocytes and T-cell tumor lines an active process of cell death called apoptosis. Interleukins (IL), including IL- 1 and IL-2, have been reported to inhibit such apoptosis. In this study we show that IL-4 also reduced the DNA fragmentation characteristic of dexamethasone (DEX)-induced apoptosis in thymocytes. This effect, studied in both time-course and dose-response experiments, was also detected at low IL-4 concentrations (1 U/mL) and against high DEX levels (10(-7) mol/L). The effect of IL-4 was blocked by an anti-IL-4 but not by an anti-IL-1 alpha MoAb, and was thus both specific and direct. Phenotypic analysis showed that IL-4 protects predominantly CD4- CD8- and CD4+CD8- cells. Our findings suggest that intrathymic T-cell development may be influenced by IL-4.


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