scholarly journals A Dual ICOS/CD28 Antagonist ICOSL Variant Ig Domain (vIgD) Potently Suppresses Human Mixed Lymphocyte Reactions and Human/NSG Mouse Xenograft Graft vs. Host Disease (GvHD)

2018 ◽  
Vol 24 (3) ◽  
pp. S187-S188
Author(s):  
Stacey R. Dillon ◽  
Katherine E. Lewis ◽  
Ryan Swanson ◽  
Lawrence S. Evans ◽  
Michael G. Kornacker ◽  
...  
Keyword(s):  
Host Disease ◽  
Mouse Xenograft ◽  
Graft Vs Host Disease ◽  
Nsg Mouse ◽  
Ig Domain ◽  
Mixed Lymphocyte Reactions

Graft-vs-leukemia activity and graft-vs-host disease induced by allogeneic Th1- and Th2-type CD4+ T cells in mice

2001 ◽  
Vol 2 (2) ◽  
pp. 136-144 ◽  
Author(s):  
Matthias Zeis ◽  
Lutz Uharek ◽  
Götz Hartung ◽  
Bertram Glass ◽  
Jörg Steinmann ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Host Disease ◽  
Graft Vs Host Disease ◽  
Th1 And Th2

scholarly journals Sudden-Onset Abdominal Pain in a 76-Year-Old Woman With Graft-vs-Host Disease

CHEST Journal ◽  
2019 ◽  
Vol 156 (4) ◽  
pp. e77-e79 ◽  
Author(s):  
Vishal J. Tolia ◽  
Danielle N. O’Hara ◽  
Kazi I. Ullah ◽  
Sahar Ahmad
Keyword(s):  
Abdominal Pain ◽  
Sudden Onset ◽  
Host Disease ◽  
Graft Vs Host Disease

scholarly journals Allosuppressor and allohelper T cells in acute and chronic graft-vs-host disease. V. F1 mice with secondary chronic GVHD contain F1-reactive allohelper but no allosuppressor T cells.

1984 ◽  
Vol 159 (2) ◽  
pp. 508-523 ◽  
Author(s):  
S T Pals ◽  
H Gleichmann ◽  
E Gleichmann
Keyword(s):  
T Cells ◽  
Early Stage ◽  
Chronic Gvhd ◽  
Third Party ◽  
Th Cells ◽  
Host Disease ◽  
Graft Vs Host Disease ◽  
Donor T Cells ◽  
Split Tolerance ◽  
B10 Cells

We studied the alloreactive properties of donor T cells obtained from F1 mice that had recovered from the allosuppression of acute graft-vs.-host disease (GVHD) and showed mild symptoms of chronic GVHD, i.e., so-called secondary chronic GVHD. To this end, we used (B10 x DBA/2)F1 mice that had been injected with 10(8) B10 spleen cells 100-150 d previously. Such GVHD F1 mice were repopulated by lympho-hematopoietic cells of donor (B10) origin, which exhibited split tolerance towards the host: Whereas F1-specific donor T helper (Th) cells as well as T cells proliferating in the mixed lymphocyte reaction were readily demonstrable, F1-specific T suppressor (Ts) and T killer (Tk) cells were not, or were hardly, detectable; responses against third-party alloantigens were normal. Upon adoptive transfer to nonirradiated secondary recipients, the B10 cells obtained from the repopulated GVH F1 mice induced F1-specific enlargement of the draining popliteal lymph node and enhancement of the IgG formation therein. B10 cells of the same kind were unable, however, to induce lethal GVHD upon transfer to 950 rad-irradiated secondary (B10 x DBA/2)F1 recipients. We conclude that alloactivated donor Ts/Tk cells disappear from the host at a relatively early stage of GVHD, i.e., at the end of acute GVHD , presumably because they are short-lived. By contrast, the longevity of alloactivated donor Th cells causes the symptoms of secondary chronic GVHD.

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