2020
DOI: 10.1182/bloodadvances.2019000853
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Postvaccination graft dysfunction/aplastic anemia relapse with massive clonal expansion of autologous CD8+ lymphocytes

Abstract: Key Points Acquired aplastic anemia is a T-cell–mediated autoimmune bone marrow aplasia, without a known etiologic trigger. Clonal expansion of CD8+ effector T lymphocytes can occur following vaccination and accompany graft dysfunction or aplastic anemia relapse.

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Cited by 17 publications
(20 citation statements)
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“…The measurement of vaccine antibody titers before and after allogeneic HSCT may provide a clue to the pathogenesis of vaccine-related autoimmune diseases. The clonal expansion of effector T cells was also reported to occur following vaccination [ 20 ]. To understand the link between COVID-19 vaccination and the development of AA, the following needs to be examined: the exploration of autoantibodies against stem cells, the role for molecular mimicry between mRNA vaccine encoded antigens and stem cells, and T-cell subset dynamics after vaccination.…”
Section: Discussionmentioning
confidence: 99%
“…The measurement of vaccine antibody titers before and after allogeneic HSCT may provide a clue to the pathogenesis of vaccine-related autoimmune diseases. The clonal expansion of effector T cells was also reported to occur following vaccination [ 20 ]. To understand the link between COVID-19 vaccination and the development of AA, the following needs to be examined: the exploration of autoantibodies against stem cells, the role for molecular mimicry between mRNA vaccine encoded antigens and stem cells, and T-cell subset dynamics after vaccination.…”
Section: Discussionmentioning
confidence: 99%
“…However, the clinical outcome seems highly unpredictable, as the other reported patients post‐HBV, H1N1 influenza, and varicella‐zoster virus vaccines were both paediatric or adults experiencing either transient disease or severe refractory AA requiring bone marrow transplant. 9 , 10 , 11 , 12 , 13 , 14 , 15 …”
mentioning
confidence: 99%
“…Previous studies on the pathogenesis of SAA have extended upstream to the activation of mDC, but the etiologic trigger for mDC is still not clear. Some cases of SAA onset or relapse after virus infection or vaccination, 5 which make many scholars believe that antigen stimulation may be the cause of mDC activation and the resulting immune response. FR Schuster, et al 6 preformed a spectratype analysis of TCR V‐beta pattern for bone marrow lymphocytes in SAA patients, which showed that CTL expanded with oligoclonal characteristics, and IST treatment can restore the diversity of TCR, suggesting that CTL expansion in patients with SAA is mediated by antigen.…”
Section: Discussionmentioning
confidence: 99%