The frequency and clinical significance of paraproteinemia in patients receiving hematopoietic stem cell (HSC) transplants were assessed. Of 66 patients with hematologic malignancies, excluding multiple myeloma who received an allogeneic or autologous HSC transplant, paraproteins were detected in 12 patients using immunoelectrophoresis. None of the patients showed paraproteinemia before HSC transplantation. The class of paraproteins most commonly seen was IgG. In 9 of these 12 patients (75%), a paraprotein was detected continuously after HSC transplantation for an average duration of 464 days, while others demonstrated a transient appearance of the protein. Paraproteinemia after HSC transplantation was not related to the stem cell source, (allograft vs. autograft), age, gender, viral infection and graft-vs.-host disease (GVHD). None of the patients developed plasma cell dyscrasia after the appearance of the paraprotein, while 1 patient developed secondary acute lymphoblastic leukemia. These findings indicate that paraproteinemia after HSC transplantation may be caused by an aberrant immune reconstitution after both allogeneic and autologous HSC transplantation. A long-term follow-up of patients with paraproteinemia after HSC transplantation is needed to confirm this finding in a larger series of patients.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1080/1042819031000139729 | DOI Listing |
Int J Mol Sci
December 2024
Clinic of Endocrinology, Diabetes and Diseases of National Center for Infertility and Endocrinology of Gender, 11000 Belgrade, Serbia.
Dual-double stem cell therapy, which integrates mesenchymal stem cells (MSCs) and hematopoietic stem cells (HSCs), represents a cutting-edge approach in regenerative medicine, particularly for conditions such as ovarian decline, premature ovarian insufficiency (POI), and induced ovarian failure. This therapy leverages the unique properties of MSCs and HSCs, enhancing tissue repair, immune modulation, and overall regenerative outcomes. MSCs, known for their ability to differentiate into various cell types, provide a supportive microenvironment and secrete bioactive molecules that promote angiogenesis and reduce inflammation.
View Article and Find Full Text PDFBlood
December 2024
UCLA Signaling Systems Laboratory, Los Angeles, California, United States.
Aging and chronic inflammation are associated with overabundant myeloid-primed multipotent progenitors (MPPs) amongst hematopoietic stem and progenitor cells (HSPCs). While HSC differentiation bias has been considered a primary cause of myeloid bias, whether it is sufficient has not been quantitatively evaluated. Here, we analyzed bone marrow data from the IκB- (Nfkbia+/-Nfkbib-/-Nfkbie-/-) mouse model of inflammation with elevated NFκB activity, which shows increased myeloid-biased MPPs.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
January 2025
Department of Liver Transplantation, Tianjin First Central Hospital, Tianjin, China; Tianjin Key Laboratory of Organ Transplantation, Tianjin First Central Hospital, Tianjin, China. Electronic address:
Background & Aims: The incidence of graft fibrosis is elevated following pediatric liver transplantation (pLT) and is influenced by cold ischemic time (CIT). Myosin light chain 9 (MYL9), a member of the myosin family, could act on hepatic stellate cells (HSCs) and induce a transition to active phase. We hypothesized that cold ischemic injury could stimulate MYL9 expression and lead to graft fibrosis.
View Article and Find Full Text PDFBlood
January 2025
Graduate School of Medicine and Frontier Biosciences, Osaka University, Japan.
The maintenance of cellular redox balance is crucial for cell survival and homeostasis and is disrupted with aging. Selenoproteins, comprising essential antioxidant enzymes, raise intriguing questions about their involvement in hematopoietic aging and potential reversibility. Motivated by our observation of mRNA downregulation of key antioxidant selenoproteins in aged human hematopoietic stem cells (HSCs) and previous findings of increased lipid peroxidation in aged hematopoiesis, we employed tRNASec gene (Trsp) knockout (KO) mouse model to simulate disrupted selenoprotein synthesis.
View Article and Find Full Text PDFJ Vis Exp
December 2024
Division of Exercise Physiology, Department of Health Professions, West Virginia University School of Medicine; Cancer Institute, West Virginia University School of Medicine; 3Department of Microbiology, Immunology, and Cell Biology, West Virginia University School of Medicine;
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!