scholarly journals T1/ST2 is preferentially expressed on murine Th2 cells, independent of interleukin 4, interleukin 5, and interleukin 10, and important for Th2 effector function

1998 ◽  
Vol 95 (12) ◽  
pp. 6930-6935 ◽  
Author(s):  
M. Lohning ◽  
A. Stroehmann ◽  
A. J. Coyle ◽  
J. L. Grogan ◽  
S. Lin ◽  
...  
Blood ◽  
1995 ◽  
Vol 85 (3) ◽  
pp. 842-851 ◽  
Author(s):  
BR Blazar ◽  
PA Taylor ◽  
S Smith ◽  
DA Vallera

Studies in mice and humans have indicated that the predominance of interleukin-4 (IL-4)- and IL-10-producing T-helper type 2 (Th2) cells may serve to downregulate acute graft-versus-host disease (GVHD) reactions, whereas IL-2-producing Th1 cells have been implicated in facilitating acute GVHD. We explored the possibility that the in vivo infusion of IL-10 would inhibit acute GVHD induced by fully allogeneic donor grafts. Unexpectedly, IL-10 infusions resulted in a dose- dependent increase in GVHD-induced mortality. The acceleration of lethal GVHD by IL-10 occurred in irradiated recipients of T-cell- depleted bone marrow (BM) plus 5, 15, or 25 x 10(6) splenocytes but did not influence the post-BM transplantation (post-BMT) survival rate of recipients of BM without splenocytes, suggesting that the IL-10 effects were not due to toxicity. Antimurine IL-10-neutralizing monoclonal antibody injections, administered to diminish endogenous IL-10, reduced GVHD-associated mortality and improved the clinical appearance of the recipients. For BM graft rejection studies, IL-10 was infused into sublethally irradiated recipients of anti-Thy 1.2 + C′ T-cell-depleted, fully allogeneic BM grafts. In a short-term (day 7) in vivo assay, IL- 10 infusions significantly inhibited allogeneic (but not syngeneic) BM proliferation in vivo, indicative of increased graft rejection. In long- term chimerism experiments, IL-10 infusions caused a significant increase in early post-BMT mortality caused by a profound anemia typically associated with graft rejection and aplasia. A slightly higher irradiation dose (650 cGy v 600 cGy) eliminated the anemia but did not reverse the graft rejection process associated with IL-10 administration. We conclude that the in vivo infusion of exogenous IL- 10 in recipients of fully allogeneic donor grafts results in accelerated GVHD and graft rejection in the strain combinations tested to date.


Science ◽  
1991 ◽  
Vol 254 (5029) ◽  
pp. 277-279 ◽  
Author(s):  
M Yamamura ◽  
K Uyemura ◽  
RJ Deans ◽  
K Weinberg ◽  
TH Rea ◽  
...  

The immunological mechanisms required to engender resistance have been defined in few infectious diseases of man, and the role of specific cytokines is unclear. Leprosy presents clinically as a spectrum in which resistance correlates with cell-mediated immunity to the pathogen. To assess in situ cytokine patterns, messenger RNA extracted from leprosy skin biopsy specimens was amplified by the polymerase chain reaction with 14 cytokine-specific primers. In lesions of the resistant form of the disease, messenger RNAs coding for interleukin-2 and interferon-gamma were most evident. In contrast, messenger RNAs for interleukin-4, interleukin-5, and interleukin-10 predominated in the multibacillary form. Thus, resistance and susceptibility were correlated with distinct patterns of cytokine production.


1997 ◽  
Vol 27 (11) ◽  
pp. 1254-1260 ◽  
Author(s):  
M. O. HOEKSTRA ◽  
Y. HOEKSTRA ◽  
D. DE REUS ◽  
B. RUTGERS ◽  
J. GERRITSEN ◽  
...  

2004 ◽  
Vol 173 (3) ◽  
pp. 1779-1786 ◽  
Author(s):  
Lianne Wassink ◽  
Pedro L. Vieira ◽  
Hermelijn H. Smits ◽  
Gillian A. Kingsbury ◽  
Anthony J. Coyle ◽  
...  

2014 ◽  
Vol 5 ◽  
Author(s):  
Piyali Chatterjee ◽  
Valorie L. Chiasson ◽  
Kelsey R. Bounds ◽  
Brett M. Mitchell

2021 ◽  
Vol 11 (6) ◽  
pp. 1091-1098
Author(s):  
Jingju Hu ◽  
Jing Yang ◽  
Hua Guo ◽  
Xuesong Yao ◽  
Haiyan Qiu ◽  
...  

To study the effect of theaflavin on the airway’s inflammation and remodeling in mice with asthma. The mice were divided into the control, asthma model, and the theaflavin treatment groups to analyze the changes in pulmonary compliance and lung resistance of the mice with asthma to theaflavin treatment. The theaflavin treatment groups consisted of the low-dose (15 mg/kg theaflavin-intragastric administration), medium-dose (30 mg/kg), and high-dose (60 mg/kg) groups. Alveoli lavage liquid was gathered from the mice to count the number of inflammatory cells, and the levels of interleukin 4 (IL-4), interleukin 5 (IL-5), interleukin 13 (IL-13), and eotaxin were detected by ELISA. The levels of proteins, such as transforming growth factor-1 (TGF-1), alpha-smooth muscle actin (α-SMA), CyclinD1,CyclinD2, Toll-like receptors-4 (TLR4), myeloid differentiation factor 88 (MyD88), and NF-κBp65, which showed the performance of lung tissue was tested by Western blotting. Compared to the control group, the lung resistance of the asthma model mice was increased, and compliance was decreased after increasing concentrations of acetylcholine (Mch) stimulation. Compared to the asthma model group, the pulmonary resistance was decreased, and pulmonar compliance was increased according to the rising concentration of Mch in theaflavin-L, theaflavin-M and theaflavin-H mice. Compared to the control group, the number of cells, macrophages, acidophilic cells, lymph, and neutrophile granulocytes increased in the alveolar perfusion fluid of asthmatic mice. The level of interleukin 4, interleukin 5, interleukin 13, and eotaxin, TGF-β1, α-SMA, Cyclin D1, MyD88, TLR4, Cyclin D2, and NF-κBp65 proteins of the lung was also increased. Compared to the model group, the number of cells, macrophages, acidophilic cells, lymph, and neutrophile granulocytes were decreased successively in the alveolar lavage fluid in the theaflavin-L, theaflavin-M, and theaflavin-H mice. Meanwhile, the content of interleukin 4, interleukin 5, interleukin 13, and eotaxin were decreased successively, and the level of TGF-β1, α-SMA, Cyclin D1, MyD88, TLR4, Cyclin D2, and NF-Bp65 protein increased successively in the theaflavin-L, theaflavin-M, and theaflavin-H mice. Theaflavin has been found to reduce airway inflammation, impede airway remodeling, and decrease the TLR 4/MyD88/NF-B signaling in asthmatic mice.


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