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.

Split tolerance to a viral antigen expressed in thymic epithelium and keratinocytes

1998 ◽  
Vol 28 (9) ◽  
pp. 2791-2800 ◽  
Author(s):  
Ian H. Frazer ◽  
Germain J. P. Fernando ◽  
Nina Fowler ◽  
Graham R. Leggatt ◽  
Paul F. Lambert ◽  
...  
Keyword(s):  
Viral Antigen ◽  
Thymic Epithelium ◽  
Split Tolerance

Split tolerance

1964 ◽  
Vol 2 (6) ◽  
pp. 807
Author(s):  
C. Martinez ◽  
J. Smith
Keyword(s):  
Split Tolerance

scholarly journals Modification of host dendritic cells by microchimerism-derived extracellular vesicles generates split tolerance

2017 ◽  
Vol 114 (5) ◽  
pp. 1099-1104 ◽  
Author(s):  
William Bracamonte-Baran ◽  
Jonathan Florentin ◽  
Ying Zhou ◽  
Ewa Jankowska-Gan ◽  
W. John Haynes ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Extracellular Vesicle ◽  
Membrane Microdomains ◽  
Transplant Tolerance ◽  
Split Tolerance ◽  
Cross Dressing

Maternal microchimerism (MMc) has been associated with development of allospecific transplant tolerance, antitumor immunity, and cross-generational reproductive fitness, but its mode of action is unknown. We found in a murine model that MMc caused exposure to the noninherited maternal antigens in all offspring, but in some, MMc magnitude was enough to cause membrane alloantigen acquisition (mAAQ; “cross-dressing”) of host dendritic cells (DCs). Extracellular vesicle (EV)-enriched serum fractions from mAAQ+, but not from non-mAAQ, mice reproduced the DC cross-dressing phenomenon in vitro. In vivo, mAAQ was associated with increased expression of immune modulators PD-L1 (programmed death-ligand 1) and CD86 by myeloid DCs (mDCs) and decreased presentation of allopeptide+self-MHC complexes, along with increased PD-L1, on plasmacytoid DCs (pDCs). Remarkably, both serum EV-enriched fractions and membrane microdomains containing the acquired MHC alloantigens included CD86, but completely excluded PD-L1. In contrast, EV-enriched fractions and microdomains containing allopeptide+self-MHC did not exclude PD-L1. Adoptive transfer of allospecific transgenic CD4 T cells revealed a “split tolerance” status in mAAQ+mice: T cells recognizing intact acquired MHC alloantigens proliferated, whereas those responding to allopeptide+self-MHC did not. Using isolated pDCs and mDCs for in vitro culture with allopeptide+self-MHC–specific CD4 T cells, we could replicate their normal activation in non-mAAQ mice, and PD-L1–dependent anergy in mAAQ+hosts. We propose that EVs provide a physiologic link between microchimerism and split tolerance, with implications for tumor immunity, transplantation, autoimmunity, and reproductive success.

SPLIT TOLERANCE INDUCED BY IMMUNOTOXIN IN A RHESUS KIDNEY ALLOGRAFT MODEL1

1997 ◽  
Vol 63 (9) ◽  
pp. 1339-1345 ◽  
Author(s):  
John H. Fechner ◽  
Daniel J. Vargo ◽  
Edward K. Geissler ◽  
Christian Graeb ◽  
Jue Wang ◽  
...  
Keyword(s):  
Kidney Allograft ◽  
Split Tolerance

Split tolerance for lymphocyte and heart allografts

1996 ◽  
Vol 5 (5) ◽  
pp. 64
Author(s):  
JASKLOWSKAENGLISZ
Keyword(s):  
Split Tolerance

scholarly journals Development of Either Split Tolerance or Robust Tolerance along with Humoral Tolerance to Donor and Third-Party Alloantigens in Nonmyeloablative Mixed Chimeras

2008 ◽  
Vol 180 (8) ◽  
pp. 5177-5186 ◽  
Author(s):  
William F. N. Chan ◽  
Haide Razavy ◽  
Bin Luo ◽  
A. M. James Shapiro ◽  
Colin C. Anderson
Keyword(s):  
Third Party ◽  
Split Tolerance ◽  
Humoral Tolerance ◽  
Mixed Chimeras

scholarly journals Differential Susceptibility of Allogeneic Targets to Indirect CD4 Immunity Generates Split Tolerance

2008 ◽  
Vol 181 (7) ◽  
pp. 4603-4612 ◽  
Author(s):  
William F. N. Chan ◽  
Haide Razavy ◽  
Colin C. Anderson
Keyword(s):  
Differential Susceptibility ◽  
Split Tolerance
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