Graft-vs-host disease (GVHD) and the sequela of immunosuppression used to prevent it remain major causes of morbidity and mortality in allogeneic stem cell transplantation (alloSCT). In particular, GVHD and ineffective T-cell immune reconstitution significantly decreases the enthusiasm for offering alloSCT to patients with non-malignant inherited hematopoietic diseases such as sickle cell anemia and thalassemia [1–6]. In GVHD, T cells that accompany the stem cell graft attack recipient tissues, including skin, liver, small and large bowel, and lung. T cells are initially primed by professional antigen-presenting cells [7,8]. In particular, dendritic cells (DCs) are uniquely specialized for uptake and presentation of antigen to nao ¨ve T cells. In the context of transplantation, this is the mechanism whereby the rare T cell with an antigen receptor (T-cell receptor; TCR) that can recognize a hostderived peptide antigen bound to MHC molecules is primed to undergo activation, clonal expansion, and maturation. This interaction is the subject of this review. While most DCs share the ability to present antigen to and stimulate nao ¨ve T cells, they are nevertheless quite heterogeneous. This heterogeneity has been the subject of recent reviews and will not be discussed in detail here [7,8]. In short, DCs differ in surface phenotype, profiles of cytokine production, location, ability to produce cytokines, and ability to present exogenously acquired antigen. Moreover, each subtype exists in an immature and a mature state. The transplant setting adds additional levels of complexity. Donorand host-derived DCs may have different roles, and what applies to presentation to CD8 cells may not apply to presentation to CD4 cells due to differences in the pathways that lead to peptide loading onto MHC I (to CD8 cells) and MHCII (to CD4 cells) [9–12]. What is true in MHC-identical transplants may differ from what is found in MHC-disparate transplants. Finally, transplant conditioning regimens and stem cell mobilization procedures may also impact APC phenotype, function, and survival.