Role of Th2 Cells in IgG4-Related Lacrimal Gland Enlargement

2010 ◽  
Vol 152 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Hiroko Kanari ◽  
Shin-ichiro Kagami ◽  
Daisuke Kashiwakuma ◽  
Yoshihiro Oya ◽  
Shunsuke Furuta ◽  
...  
Science ◽  
1993 ◽  
Vol 260 (5116) ◽  
pp. 1931-1934 ◽  
Author(s):  
A. Taylor-Robinson ◽  
R. Phillips ◽  
A Severn ◽  
S Moncada ◽  
F. Liew

2018 ◽  
Vol 257 (2) ◽  
pp. 405-411 ◽  
Author(s):  
Eri Ishikawa ◽  
Yasuhiro Takahashi ◽  
Ma. Regina Paula Valencia ◽  
Marian Grace Ana-Magadia ◽  
Hirohiko Kakizaki

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Anouk K. Gloudemans ◽  
Bart N. Lambrecht ◽  
Hermelijn H. Smits

Allergic asthma is characterized by bronchial hyperresponsiveness, a defective barrier function, and eosinophilic lower airway inflammation in response to allergens. The inflammation is dominated by Th2 cells and IgE molecules and supplemented with Th17 cells in severe asthma. In contrast, in healthy individuals, allergen-specific IgA and IgG4 molecules are found but no IgE, and their T cells fail to proliferate in response to allergens, probably because of the development of regulatory processes that actively suppress responses to allergens. The presence of allergen-specific secretory IgA has drawn little attention so far, although a few epidemiological studies point at a reverse association between IgA levels and the incidence of allergic airway disease. This review highlights the latest literature on the role of mucosal IgA in protection against allergic airway disease, the mechanisms described to induce secretory IgA, and the role of (mucosal) dendritic cells in this process. Finally, we discuss how this information can be used to translate into the development of new therapies for allergic diseases based on, or supplemented with, IgA boosting strategies.


2002 ◽  
Vol 283 (1) ◽  
pp. L198-L204 ◽  
Author(s):  
Jane M. Schuh ◽  
Kate Blease ◽  
Steven L. Kunkel ◽  
Cory M. Hogaboam

Eotaxin/CCL11 is a major chemoattractant for eosinophils and Th2 cells. As such, it represents an attractive target in the treatment of allergic disease. The present study addresses the role of eotaxin/CCL11 during acute and chronic allergic airway responses to the fungus Aspergillus fumigatus. Mice lacking the eotaxin gene (Eo−/−) and wild-type mice (Eo+/+) were sensitized to A. fumigatus and received either an intratracheal challenge with soluble A. fumigatusantigens (acute model) or an intratracheal challenge with live A. fumigatus spores or conidia (chronic model). Airway hyperresponsiveness and eosinophil, but not T cell, recruitment were significantly decreased at 24 h after the soluble allergen in A. fumigatus-sensitized Eo−/− mice compared with similarly sensitized Eo+/+ mice. In contrast, the development of chronic allergic airway disease due to A. fumigatus conidia was not altered by the lack of eotaxin. Together, these data suggest that eotaxin initiates allergic airway disease due to A. fumigatus, but this chemokine did not appear to contribute to the maintenance of A. fumigatus-induced allergic airway disease.


2021 ◽  
Author(s):  
Aftab Alam ◽  
Maulasri Bhatta ◽  
Parker Denz ◽  
Eric Levanduski ◽  
Prasenjit Dey

Author(s):  
Om Sharma ◽  
Violeta Mihailovic-Vucinic

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