NDLI: Ikaros deficiency in host hematopoietic cells separates GVL from GVHD after experimental allogeneic hematopoietic cell transplantation

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Ikaros deficiency in host hematopoietic cells separates GVL from GVHD after experimental allogeneic hematopoietic cell transplantation

Content Provider	PubMed Central
Author	Toubai, Tomomi Hou, Guoqing Rossi, Corrine Mathewson, Nathan Katherine, Oravecz-wilson Cummings, Emily Wu, Julia Sun, Yaping Choi, Sung Reddy, Pavan
Copyright Year	2015
Abstract	The graft-versus-leukemia (GVL) effect following allogeneic hematopoietic stem cell transplantation (allo-HCT) is critical for its curative potential. Hwever, GVL is tightly linked to graft-versus-host disease (GVHD). Among hematological malignancies, acute lymphoblastic leukemia (ALL) is the most resistant to GVL, although the reasons for this remain poorly understood. Clinical studies have identified alterations in Ikaros (Ik) transcription factor as the major marker associated with poor outcomes in ALL. We have shown that the absence of Ik in professional host-derived hematopoietic antigen-presenting cells (APCs) exacerbates GVHD. However, whether Ik expression plays a role in resistance to GVL is not known. In this study we used multiple clinically relevant murine models of allo-HCT to explore whether Ik expression in hematopoietic APCs and/or leukemic cells is critical for increasing resistance to GVL and thus inducing relapse. We found that Ik deficiency in host APCs failed to enhance GVL despite increased GVHD severity. Mechanistic studies with bone marrow (BM) chimeras and tetramer analyses demonstrated reduced tumor-specific immunodominant (gag+) antigen responses in the [B6Ik −/−→B6] group. Loss of GVL was observed when both the leukemia cells and the host APCs were deficient in Ik. We found that calreticulin (CRT) expression in host antigen-presenting dendritic cells (DCs) of Ik −/− animals was significantly lower than in wild-type animals. Rescuing CRT expression in Ik −/− DCs improved leukemic-specific cytotoxic T cell function. Together, our data demonstrate that the absence of Ikaros in host hematopoietic cells promotes resistance to GVL despite increasing GVHD and thus provides a potential mechanism for the poor outcome of Ik −/− ALL patients.
Related Links	http://dx.doi.org/10.1080/2162402X.2015.1016699
Starting Page	1016699
File Format	PDF
ISSN	2162402X
e-ISSN	2162402X
Journal	Oncoimmunology
Issue Number	7
Volume Number	4
Language	English
Publisher	Taylor & Francis
Publisher Date	2015-07-01
Access Restriction	Open
Rights Holder	Taylor & Francis
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Oncology

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