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      Post–hematopoietic stem cell transplantation immune-mediated anemia: a literature review and novel therapeutics

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          Abstract

          Anemia after allogeneic hematopoietic stem cell transplantation (HSCT) can be immune or non–immune mediated. Auto- or alloimmunity resulting from blood group incompatibility remains an important cause in post-HSCT immune-mediated anemia. ABO incompatibility is commonly encountered in HSCT and may lead to serious clinical complications, including acute hemolysis, pure red cell aplasia, and passenger lymphocyte syndrome. It remains controversial whether ABO incompatibility may affect HSCT outcomes, such as relapse, nonrelapse mortality, graft-versus-host disease, and survival. Non-ABO incompatibility is less frequently encountered but can have similar complications to ABO incompatibility, causing adverse clinical outcomes. It is crucial to identify the driving etiology of post-HSCT anemia in order to prevent and treat this condition. This requires a comprehensive understanding of the mechanism of anemia in blood group–incompatible HSCT and the temporal association between HSCT and anemia. In this review, we summarize the literature on post-HSCT immune-mediated anemia with a focus on ABO and non-ABO blood group incompatibility, describe the underlying mechanism of anemia, and outline preventive and treatment approaches.

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          Daratumumab depletes CD38+ immune regulatory cells, promotes T-cell expansion, and skews T-cell repertoire in multiple myeloma.

          Jakub Krejcik, Tineke Casneuf, Inger S Nijhof … (2016)
          Daratumumab targets CD38-expressing myeloma cells through a variety of immune-mediated mechanisms (complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and antibody-dependent cellular phagocytosis) and direct apoptosis with crosslinking. These mechanisms may also target nonplasma cells that express CD38, which prompted evaluation of daratumumab's effects on CD38-positive immune subpopulations. Peripheral blood (PB) and bone marrow (BM) from patients with relapsed/refractory myeloma from 2 daratumumab monotherapy studies were analyzed before and during therapy and at relapse. Regulatory B cells and myeloid-derived suppressor cells, previously shown to express CD38, were evaluated for immunosuppressive activity and daratumumab sensitivity in the myeloma setting. A novel subpopulation of regulatory T cells (Tregs) expressing CD38 was identified. These Tregs were more immunosuppressive in vitro than CD38-negative Tregs and were reduced in daratumumab-treated patients. In parallel, daratumumab induced robust increases in helper and cytotoxic T-cell absolute counts. In PB and BM, daratumumab induced significant increases in CD8(+):CD4(+) and CD8(+):Treg ratios, and increased memory T cells while decreasing naïve T cells. The majority of patients demonstrated these broad T-cell changes, although patients with a partial response or better showed greater maximum effector and helper T-cell increases, elevated antiviral and alloreactive functional responses, and significantly greater increases in T-cell clonality as measured by T-cell receptor (TCR) sequencing. Increased TCR clonality positively correlated with increased CD8(+) PB T-cell counts. Depletion of CD38(+) immunosuppressive cells, which is associated with an increase in T-helper cells, cytotoxic T cells, T-cell functional response, and TCR clonality, represents possible additional mechanisms of action for daratumumab and deserves further exploration.
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            National Institutes of Health consensus development project on criteria for clinical trials in chronic graft-versus-host disease: I. Diagnosis and staging working group report.

            Alexandra H. Filipovich, Daniel Weisdorf, Steven Zivko Pavletic … (2005)
            This consensus document is intended to serve 3 functions. First, it standardizes the criteria for diagnosis of chronic graft-versus-host disease (GVHD). Second, it proposes a new clinical scoring system (0-3) that describes the extent and severity of chronic GVHD for each organ or site at any given time, taking functional impact into account. Third, it proposes new guidelines for global assessment of chronic GVHD severity that are based on the number of organs or sites involved and the degree of involvement in affected organs (mild, moderate, or severe). Diagnosis of chronic GVHD requires the presence of at least 1 diagnostic clinical sign of chronic GVHD (e.g., poikiloderma or esophageal web) or the presence of at least 1 distinctive manifestation (e.g., keratoconjunctivitis sicca) confirmed by pertinent biopsy or other relevant tests (e.g., Schirmer test) in the same or another organ. Furthermore, other possible diagnoses for clinical symptoms must be excluded. No time limit is set for the diagnosis of chronic GVHD. The Working Group recognized 2 main categories of GVHD, each with 2 subcategories. The acute GVHD category is defined in the absence of diagnostic or distinctive features of chronic GVHD and includes (1) classic acute GVHD occurring within 100 days after transplantation and (2) persistent, recurrent, or late acute GVHD (features of acute GVHD occurring beyond 100 days, often during withdrawal of immune suppression). The broad category of chronic GVHD includes (1) classic chronic GVHD (without features or characteristics of acute GVHD) and (2) an overlap syndrome in which diagnostic or distinctive features of chronic GVHD and acute GVHD appear together. It is currently recommended that systemic therapy be considered for patients who meet criteria for chronic GVHD of moderate to severe global severity.
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              The SYK tyrosine kinase: a crucial player in diverse biological functions.

              Jürgen Ruland, Attila Mócsai, Victor L. J. Tybulewicz (2010)
              Spleen tyrosine kinase (SYK) is known to have a crucial role in adaptive immune receptor signalling. However, recent reports indicate that SYK also mediates other, unexpectedly diverse biological functions, including cellular adhesion, innate immune recognition, osteoclast maturation, platelet activation and vascular development. SYK is activated by C-type lectins and integrins, and activates new targets, including the CARD9-BCL-10-MALT1 pathway and the NLRP3 inflammasome. Studies using Drosophila melanogaster suggest that there is an evolutionarily ancient origin of SYK-mediated signalling. Moreover, SYK has a crucial role in autoimmune diseases and haematological malignancies. This Review summarizes our current understanding of the diverse functions of SYK and how this is being translated for therapeutic purposes.
              Article 0 comments Cited 218 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Blood Adv
                Journal ID (iso-abbrev): Blood Adv
                Journal ID (hwp): bloodoa
                Journal ID (publisher-id): Blood Advances
                Title: Blood Advances
                Publisher: American Society of Hematology (Washington, DC )
                ISSN (Print): 2473-9529
                ISSN (Electronic): 2473-9537
                Publication date Collection: 26 April 2022
                Publication date (Electronic): 26 April 2022
                Volume: 6
                Issue: 8
                Pages: 2707-2721
                Affiliations
                [1 ]Knight Cancer Institute, Oregon Health and Science University, Portland, OR;
                [2 ]National Heart, Lung, and Blood Institute, and
                [3 ]Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD; and
                [4 ]Division of Blood and Marrow Transplantation, Department of Medicine, Stanford University, Stanford, CA
                Author notes
                Correspondence: Yazan Migdady, 3181 SW Sam Jackson Park Rd, Portland, OR 97239; e-mail: migdady@ 123456ohsu.edu .
                Author information
                https://orcid.org/0000-0001-8216-7709
                https://orcid.org/0000-0002-8934-8251
                https://orcid.org/0000-0003-1993-4172
                Article
                Publisher ID: 2022/ADV2021006279
                DOI: 10.1182/bloodadvances.2021006279
                PMC ID: 9043947
                PubMed ID: 34972204
                SO-VID: abbcbd76-5c41-4ebd-a93d-7ad72f19e684
                Copyright © Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) , permitting only noncommercial, nonderivative use with attribution. All other rights reserved.
                History
                Date received : 20 October 2021
                Date accepted : 23 December 2021
                Date: 31 December 2021
                Page count
                Pages: 15
                Categories
                Subject: 5
                Subject: 22
                Subject: 28
                Subject: 30
                Subject: 31
                Subject: Review Article

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