The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fischer, A. C.
Right arrow Articles by Hess, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fischer, A. C.
Right arrow Articles by Hess, A.

The Journal of Immunology, Vol 143, Issue 3 827-832, Copyright © 1989 by American Association of Immunologists

ARTICLES

Host resistance to cyclosporine induced syngeneic graft-versus-host disease. Requirement for two distinct lymphocyte subsets

AC Fischer, MK Laulis, L Horwitz, WE Beschorner and A Hess
Oncology Center, Johns Hopkins University, Baltimore, MD 21205.

Cyclosporine is crucial for the prevention of organ allograft rejection and allogeneic graft-vs-host disease (GVHD). Despite its potent immunosuppressive activity, cyclosporine elicits a T cell-mediated autoimmune syndrome after autologous or syngeneic bone marrow transplantation, which has been termed syngeneic GVHD (SGVHD). Recent studies have shown that for disease manifestation, a cytoxan and radiation-sensitive T cell dependent host resistance mechanism must be eliminated, allowing the clonal expansion of autoreactive cells. This report characterizes the autoregulatory lymphocyte population, present in normal animals, capable of inhibiting the adoptive transfer of SGVHD. First, twice the number of unfractionated splenocytes from normal animals to those from autoimmune donors ensured complete inhibition of the adoptive transfer of immune reactivity. Second, the phenotype of this host resistance mechanism in normal splenocytes involves dual regulatory T cell subsets. A helper/inducer subset (W3/25+) must be cotransferred with a cytotoxic/suppressor subset (OX8+) in a ratio that approximates the normal ratio in normal unfractionated splenocytes in order to affect inhibition of the transfer of SGVHD. Moreover the specific inducer regulatory activity resides in the OX22-, W3/25+ subset of Th cells.


This article has been cited by other articles:


Home page
 J. Leukoc. Biol.Home page
J. S. Bryson, C. D. Jennings, J. A. Brandon, J. Perez, B. E. Caywood, and A. M. Kaplan
Adoptive transfer of murine syngeneic graft-vs.-host disease by CD4+ T cells
J. Leukoc. Biol., December 1, 2007; 82(6): 1393 - 1400.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
D. L. Flanagan, C. D. Jennings, and J. S. Bryson
Th1 Cytokines and NK Cells Participate in the Development of Murine Syngeneic Graft-Versus-Host Disease
J. Immunol., August 1, 1999; 163(3): 1170 - 1177.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
T. Guillaume, D. B. Rubinstein, and M. Symann
Immune Reconstitution and Immunotherapy After Autologous Hematopoietic Stem Cell Transplantation
Blood, September 1, 1998; 92(5): 1471 - 1490.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1989 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1989 by The American Association of Immunologists, Inc. All rights reserved.