Ex vivo simulation of IgG Fc and T-cell receptor functions: An application to inflammatory bowel disease

2008 ◽  
Vol 14 (8) ◽  
pp. 1061-1067 ◽  
Author(s):  
Masato Mitsuhashi ◽  
Stephan R. Targan
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
T Cell Receptor ◽  
Bowel Disease ◽  
Ex Vivo ◽  
Cell Receptor ◽  
Inflammatory Bowel

scholarly journals Alteration of Interleukin 4 Production Results in the Inhibition of T Helper Type 2 Cell–Dominated Inflammatory Bowel Disease in T Cell Receptor α Chain–Deficient Mice

1999 ◽  
Vol 190 (5) ◽  
pp. 607-616 ◽  
Author(s):  
Hideki Iijima ◽  
Ichiro Takahashi ◽  
Daisuke Kishi ◽  
Jin-Kyung Kim ◽  
Sunao Kawano ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Bowel Disease ◽  
Cell Receptor ◽  
Interleukin 4 ◽  
T Helper ◽  
Inflammatory Bowel ◽  
Α Chain

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.

scholarly journals Cryptosporidium parvum Initiates Inflammatory Bowel Disease in Germfree T Cell Receptor-α-Deficient Mice

1998 ◽  
Vol 153 (6) ◽  
pp. 1717-1722 ◽  
Author(s):  
Randy E. Sacco ◽  
Joseph S. Haynes ◽  
James A. Harp ◽  
W. Ray Waters ◽  
Michael J. Wannemuehler
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
T Cell Receptor ◽  
Cryptosporidium Parvum ◽  
Bowel Disease ◽  
Cell Receptor ◽  
Inflammatory Bowel ◽  
Deficient Mice

Spontaneous development of inflammatory bowel disease in T cell receptor mutant mice

Cell ◽  
1993 ◽  
Vol 75 (2) ◽  
pp. 275-282 ◽  
Author(s):  
Peter Mombaerts ◽  
Emiko Mizoguchi ◽  
Michael J. Grusby ◽  
Laurie H. Glimcher ◽  
Atul K. Bhan ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
T Cell Receptor ◽  
Bowel Disease ◽  
Cell Receptor ◽  
Mutant Mice ◽  
Inflammatory Bowel ◽  
Receptor Mutant

Immunohistochemical characterization, distribution, and ultrastructure of lymphocytes bearing T-cell receptor γ/δ in inflammatory bowel disease

1991 ◽  
Vol 101 (3) ◽  
pp. 670-678 ◽  
Author(s):  
Kouhei Fukushima ◽  
Takayuki Masuda ◽  
Haruo Ohtani ◽  
Iwao Sasaki ◽  
Yuji Funayama ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
T Cell Receptor ◽  
Bowel Disease ◽  
Cell Receptor ◽  
Inflammatory Bowel
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