title: Biologic markers of chronic GVHD.
abstract: Biologic markers of chronic GVHD may provide insight into the pathogenesis of the syndrome, identify molecular targets for novel interventions, and facilitate advances in clinical management. Despite extensive work performed to date largely focused on prediction and diagnosis of the syndrome, little synthesis of findings and validation of promising candidate markers in independent populations has been performed. Studies suggest that risk for subsequent chronic GVHD development may be associated with donor-recipient genetic polymorphism, deficiency in regulatory immune cell populations (NK, Treg, DC2), and variation in inflammatory and immunoregulatory mediators post-HCT (increased TNFα, IL-10 and BAFF, and decreased TGFβ and IL-15). Established chronic GVHD is associated with alteration in immune cell populations (increased CD3(+) T cells, Th17, CD4(+) and CD8(+) effector memory cells, monocytes, CD86 expression, BAFF/B cell ratio, and deficiency of Treg, NK cells, and naïve CD8(+) T cells). Inflammatory and immunomodulatory factors (TNFα, IL-6, IL-1β, IL-8, sIL-2R, and IL-1Ra, BAFF, anti-dsDNA, sIL-2Rα, and sCD13) are also perturbed. Little is known about biologic markers of chronic GVHD phenotype and severity, response to therapy, and prognosis.
authors.affiliation: Blood and Marrow Transplantation, Moffitt Cancer Center, Tampa, FL, USA.
authors.forename: J
authors.initials: J
authors.lastname: Pidala
authors.affiliation: Transplant Nephrology and Pediatrics, BIOMARC Institute for Personalized Medicine, California Pacific Medical Center, San Francisco, CA, USA.
authors.forename: M
authors.initials: M
authors.lastname: Sarwal
authors.affiliation: BIOMARC Institute for Personalized Medicine, California Pacific Medical Center, San Francisco, CA, USA.
authors.forename: S
authors.initials: S
authors.lastname: Roedder
authors.affiliation: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
authors.forename: S J
authors.initials: SJ
authors.lastname: Lee
mesh_terms: D053264:B-Cell Activating Factor / Q000378:metabolism; D015415:Biomarkers / Q000097:blood* / Q000378:metabolism*; D017252:CD3 Complex / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology; D006086:Graft vs Host Disease / Q000097:blood* / Q000276:immunology*; D006801:Humans; D007249:Inflammation; D016753:Interleukin-10 / Q000378:metabolism; D019409:Interleukin-15 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000166:cytology; D010641:Phenotype; D011110:Polymorphism, Genetic; D058504:Th17 Cells / Q000166:cytology; D014019:Tissue Donors; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053264:B-Cell Activating Factor; D015415:Biomarkers; D017252:CD3 Complex; D019409:Interleukin-15; C505719:TNFSF13B protein, human; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10