TY - JOUR
T1 - Cutting edge
T2 - A monoclonal antibody specific for the programmed death-1 homolog prevents graft-versus-host disease in mouse models
AU - Flies, Dallas B.
AU - Wang, Shengdian
AU - Xu, Haiying
AU - Chen, Lieping
PY - 2011/8/15
Y1 - 2011/8/15
N2 - Upon interaction with B7 homolog 1, programmed death-1 (PD-1) transmits a critical coinhibitory signal to T cells to negatively regulate immune responses. By extensively searching the genomic database with the IgV region of PD-1, we identified a homolog and named it PD-1 homolog (PD-1H). PD-1H is broadly expressed on the cell surface of hematopoietic cells and could be further upregulated on CD4+ and CD8+ T cells following activation. We have generated an mAb against PD-1H, which strikingly prevents acute graft-versus-host disease in semi- and fully allogeneic murine models, leading to full chimerism following treatment. Graft-versus-host disease remains a primary hindrance to successful allogeneic hematopoietic cell transplantation therapy for the treatment of hematologic malignancy. Therefore, manipulation of PD-1H function may provide a new modality for controlling T cell responses to allogeneic tissues in transplant medicine.
AB - Upon interaction with B7 homolog 1, programmed death-1 (PD-1) transmits a critical coinhibitory signal to T cells to negatively regulate immune responses. By extensively searching the genomic database with the IgV region of PD-1, we identified a homolog and named it PD-1 homolog (PD-1H). PD-1H is broadly expressed on the cell surface of hematopoietic cells and could be further upregulated on CD4+ and CD8+ T cells following activation. We have generated an mAb against PD-1H, which strikingly prevents acute graft-versus-host disease in semi- and fully allogeneic murine models, leading to full chimerism following treatment. Graft-versus-host disease remains a primary hindrance to successful allogeneic hematopoietic cell transplantation therapy for the treatment of hematologic malignancy. Therefore, manipulation of PD-1H function may provide a new modality for controlling T cell responses to allogeneic tissues in transplant medicine.
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U2 - 10.4049/jimmunol.1100660
DO - 10.4049/jimmunol.1100660
M3 - Article
C2 - 21768399
AN - SCOPUS:80051930238
SN - 0022-1767
VL - 187
SP - 1537
EP - 1541
JO - Journal of Immunology
JF - Journal of Immunology
IS - 4
ER -