Tissue distribution of MiHAs. Gene expression analysis was performed to distinguish hematopoietic-restricted MiHAs from MiHAs that are broadly expressed or at higher levels in nonhematopoietic tissues. (A) In the single cell section of the HPA, gene expression was reported for 123 of 129 genes coding for 159 MiHAs. Highest gene expression values (nTPM, normalized transcripts per million) for each MiHA in nonhematopoietic (nonhem) and hematopoietic cell clusters (hem) present in tissues involved in GVHD were compared (inner circle: nonhematopoietic cells in skin, esophagus, stomach, small intestine, colon, rectum, liver, lung, bronchus, eye and thymus; second circle: hematopoietic cells including B cells, plasma cells, T cells, natural killer cells, monocytes, dendritic cells, macrophages, Langerhans cells, Kupffer cells, granulocytes, erythroid cells, platelets, and mixed immune cells in GVHD tissues as well as PBMCs and spleen). Cell clusters of undefined mixed cell types were excluded. The maximum expression value in hematopoietic cells (inner lane, third circle) was compared to the maximum value (outer lane, third circle) in nonhematopoietic cell clusters. Genes were grouped based on the calculated ratio (H/NH; outer circle). (B) Indicated is the number of targeted MiHAs in the 39 patients, colored based on their gene expression profiles as defined in panel A. MiHAs with lacking gene expression data are displayed in gray. (C) Microarray data from healthy and malignant hematopoietic cells as well as nonhematopoietic cells cultured under inflammatory conditions were used to analyze gene expression of 20 genes with a ratio ≥5 in hematopoietic cells in the HPA data set. No conclusion could be drawn for 2 genes (CCL4 and BCL2A1) with insufficient probe fluorescence. Of the remaining 18 genes, 11 genes coding for 14 MiHAs showed low expression in nonhematopoietic cell types and therefore have potential as targets for immunotherapy to stimulate GVL reactivity after alloSCT without GVHD (group 1). The other 7 genes showed high expression in ≥1 nonhematopoietic cell types (group 2). DC, dendritic cells; HUVEC, human umbilical vein endothelial cells; PTEC, proximal tubular epithelial cells; sup, supernatant.

Tissue distribution of MiHAs. Gene expression analysis was performed to distinguish hematopoietic-restricted MiHAs from MiHAs that are broadly expressed or at higher levels in nonhematopoietic tissues. (A) In the single cell section of the HPA, gene expression was reported for 123 of 129 genes coding for 159 MiHAs. Highest gene expression values (nTPM, normalized transcripts per million) for each MiHA in nonhematopoietic (nonhem) and hematopoietic cell clusters (hem) present in tissues involved in GVHD were compared (inner circle: nonhematopoietic cells in skin, esophagus, stomach, small intestine, colon, rectum, liver, lung, bronchus, eye and thymus; second circle: hematopoietic cells including B cells, plasma cells, T cells, natural killer cells, monocytes, dendritic cells, macrophages, Langerhans cells, Kupffer cells, granulocytes, erythroid cells, platelets, and mixed immune cells in GVHD tissues as well as PBMCs and spleen). Cell clusters of undefined mixed cell types were excluded. The maximum expression value in hematopoietic cells (inner lane, third circle) was compared to the maximum value (outer lane, third circle) in nonhematopoietic cell clusters. Genes were grouped based on the calculated ratio (H/NH; outer circle). (B) Indicated is the number of targeted MiHAs in the 39 patients, colored based on their gene expression profiles as defined in panel A. MiHAs with lacking gene expression data are displayed in gray. (C) Microarray data from healthy and malignant hematopoietic cells as well as nonhematopoietic cells cultured under inflammatory conditions were used to analyze gene expression of 20 genes with a ratio ≥5 in hematopoietic cells in the HPA data set. No conclusion could be drawn for 2 genes (CCL4 and BCL2A1) with insufficient probe fluorescence. Of the remaining 18 genes, 11 genes coding for 14 MiHAs showed low expression in nonhematopoietic cell types and therefore have potential as targets for immunotherapy to stimulate GVL reactivity after alloSCT without GVHD (group 1). The other 7 genes showed high expression in ≥1 nonhematopoietic cell types (group 2). DC, dendritic cells; HUVEC, human umbilical vein endothelial cells; PTEC, proximal tubular epithelial cells; sup, supernatant.

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