Transient Elevation of Serum IgE after Allogeneic Bone-Marrow Transplantation

Korver, K.; Schellekens, P. T. A.; Dooren, L. J.; Vossen, Jaak M.

doi:10.1159/000234397

Cited by 11 publications

(4 citation statements)

References 30 publications

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“…29 Second, elevation in total IgE is known to occur following BMT; however, this appears to be a transient phenomenon that occurs early after BMT without long-term persistence. 30,31 Other diagnoses could mimic asthma in this patient population, especially BO syndrome in those with GVHD. However, this is unlikely to have confounded the results of this study because all patients with asthma reported allergic triggers for their asthma symptoms and BO was specifically excluded in 1 of the 2 patients with chronic GVHD.…”

Section: Discussionmentioning

confidence: 91%

Long-term acquisition of allergen-specific IgE and asthma following allogeneic bone marrow transplantation from allergic donors

Hallstrand

Sprenger

Agosti

et al. 2004

Blood

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Adoptive transfer of allergen-specific immunoglobulin E (IgE) from atopic donors to nonatopic recipients occurs during the first year following bone marrow transplantation (BMT). Mature B-and T-cell clones with allergen-specific memory and hematopoietic progenitor cells are transferred through BMT. The objective of this study was to characterize the long-term rate of allergic sensitization and development of clinical allergic diseases following BMT from atopic donors. A long-term follow-up study was conducted in a cohort of donor and recipient pairs with moderate-to-severe allergic disease in the donor prior to BMT. Assessments of allergen-specific IgE, clinical rhinitis, and asthma were made in the donors prior to BMT and in the recipients with a mean follow-up of 15.5 years after BMT. From an initial cohort of 12 bone marrow transplant recipients who received marrow from allergic donors, 5 long-term survivors were identified. Allergen-specific IgE transferred from donor to recipient following BMT frequently persisted, and a high rate of de novo allergic sensitization was observed between 1 and 14 years after BMT. These events were associated with elevation in total IgE, and development of allergic rhinitis and asthma at long-term follow-up. We conclude that marrowderived immune cells from allergic donors can transfer the predisposition to allergy and asthma. IntroductionAsthma and allergic diseases result from genetic and environmental influences. A unique opportunity to understand the development of asthma and allergy occurs during bone marrow transplantation (BMT) when recipients without allergic disease receive immune cells from allergic donors. We previously showed that recipients undergoing BMT from donors with moderate-to-severe allergic disease had a high rate of acquisition of donor allergen-specific immunoglobulin E (IgE) in the first year after transplantation consistent with adoptive transfer of B-and/or helper T-cell clones with allergen-specific memory. 1 Although our previous study and a number of case reports 2-6 have documented adoptive transfer of allergen-specific IgE in the first year following BMT from atopic donors, there are no long-term studies identifying the consequences of this initial adoptive transfer of allergen-specific IgE and immune cells during BMT from atopic donors. We conducted a long-term follow-up study more than 14 years after BMT in the same cohort of recipients that had received bone marrow transplants from donors with moderate-to-severe allergic disease and determined the long-term persistence of the IgE response and development of clinical allergic disease in recipients. We found that recipients had a high rate of persistence of transferred allergen-specific IgE, and acquisition of new allergen-specific IgE, elevated total IgE, allergic rhinitis, and asthma. This study suggests that marrow-derived immune cells transfer the predisposition to allergy and asthma and supports the primary role of immune cells in the development of the asthma phenotype. Patients, materials...

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Section: Discussionmentioning

confidence: 91%

Long-term acquisition of allergen-specific IgE and asthma following allogeneic bone marrow transplantation from allergic donors

Hallstrand

Sprenger

Agosti

et al. 2004

Blood

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“…Mean serum IgD levels or the proportion of individuals with high levels of IgD were increased in a variety of disorders with immune activation and immunodeficiencies, usually associated with increases in other immunoglobulin isotypes. However, a significant number of individuals had low levels in these disorders which included HIV infection [8][9][10], chronic bronchopulmonary aspergillosis [11], Down's syndrome [12], acute hepatitis and salmonellosis [13], atopies [14], chronic obstructive pulmonary disease [15] and hyper-IgE syndrome [16,17], This was also the case in disorders not usually associated with other forms o f hypergammaglobuli nemia such as Hodgkin's disease [18], tuberculosis [19], in children following chemotherapy for malignancy [20], and after bone marrow transplantation [21]. Even in one disor der defined by high levels of IgD, the hyper-IgD syndrome, normal levels were occasionally observed [22], Significant ly decreased levels were observed in some immunoglobulin deficiency states-non-X-linked agammaglobulinemia [17] and IgA deficiency [17,23].…”

Section: Introductionmentioning

confidence: 99%

Serum IgD Levels in Children under Investigation for and with Defined Immunodeficiency

Litzman

Ward

Wild

et al. 1997

Int Arch Allergy Immunol

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Background: The function and regulation of circulating IgD are unclear. Serum IgD levels were increased in a wide range of immunological diseases but these associations did not give a clue to the regulation of serum IgD production. Methods: Serum IgD levels in 131 children with various non-HIV-related immunodeficiency diseases were investigated to examine their relationship with immunoglobulin or antibody production and activation of the immune system. Data from a group of 109 nonimmunodefícient children were also available for comparison. Results: There was a bimodal distribution of serum IgD levels. In 87 patients IgD levels fell below the limit of detection of 5 IU/ml, while the remainder showed an approximately normal distribution skewed to the right after log transformation. The proportion of children with undetectable IgD levels (< 5 IU/ml) was significantly increased in immunodeficient children (87/131 vs. 28/109, p < 0.001). No difference in the occurrence of immunoglobulin or antibody deficiencies was demonstrated in immunodeficient children with detectable and non-detectable IgD levels. There was a positive correlation of serum IgD with age, serum IgA and IgE, white blood count and CD4+CD25+ lymphocytes but not with other immunoglobulin isotypes or immune activation markers. Conclusion: Determination of serum IgD levels did not seem to be of particular clinical benefit in the investigation of HIV-negative immunodeficient children and serum IgD levels were not associated with the general picture of immune activation. Observed distribution patterns and associations may have implications for the regulation of serum IgD production.

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“…Furthermore, IgE levels are often raised in recipients receiving marrow from non‐atopic donors [6]. The evidence that serum IgE levels rise with the onset of GvHD or infection is conflicting; some studies report an association, whilst others demonstrate no temporal correlation [7, 8]. The rise is not related to myeloablative chemotherapy as it has been observed in immunodeficient children transplanted without chemotherapy [9].…”

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confidence: 99%

“…Serum IgE rise is preceded by an increase in a soluble CD23 product, thought to be a fragment of the low‐affinity IgE receptor, and probably released during the immunoregulatory imbalance immediately post‐transplantation [10]. In the immediate post‐transplant period it is likely that donor‐derived IgE‐secreting mature B cells are released from the normal T cell regulation, allowing an uncontrolled release of IgE, until regulatory T cells have re‐populated [8]. However, GvHD is characterized by cellular degeneration and damage, mediated by activated macrophages and a Th1‐type response [11].…”

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confidence: 99%