Regulation of human immunoglobulin E synthesis in acute graft versus host disease.

Saryan, John A.; Rappeport, Joel M.; Leung, Donald Y.M.; Parkman, Robertson; Geha, Raif S.

doi:10.1172/jci110800

Cited by 43 publications

(6 citation statements)

References 23 publications

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“…IgE elevations after BMT have been attributed to the occurrence of clinically acute GvHD [3][4][5][6]23] and the suggestion was made that measurement of serum IgE could be useful for monitoring this syndrome [5]. Our results do not support these assumptions.…”

Section: Discussioncontrasting

confidence: 78%

“…This complication has been found to be associated with T-cell immunoregulatory dis turbance [51][52][53]. The concomittant occurrence of clinically acute GvHD and IgE peaks, as found in some studies, including enhanced in vitro IgE synthe sis [23], is net in contradiction with an underlying Tcell disregulation as the most important mechanism. It is possible that an 'allogeneic effect', i.e.…”

Section: Discussionmentioning

confidence: 99%

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Transient Elevation of Serum IgE after Allogeneic Bone-Marrow Transplantation

Korver

Schellekens

Dooren

et al. 1987

Int Arch Allergy Immunol

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Serum IgE levels were followed longitudinally twice a week for up to 100 days in 60 children treated for leukemia, severe aplastic anemia or severe combined immunodeficiency: 52 underwent allogeneic bone-marrow transplantation and 8 immunosuppressive treatment. In 55 of 58 treatment periods which could be analyzed (95%), a transient sharp increase of serum IgE was detected, irrespective of the initial diagnosis and mode of treatment. A second IgE peak was recorded in 16% of evaluable treatment periods. In the transplanted leukemia and aplastic anemia patients, the rise of serum IgE levels occurred at the same time, i.e. at a mean of 14 days after transplantation; it occurred significantly later in children grafted for severe combined immunodeficiency. In children who received immunosuppression for the treatment of severe aplastic anemia, IgE elevations were always seen within 2 weeks after institution of therapy. No relation was found between either the occurrence of clinically acute graft-versus-host disease or infections after treatment, and the time of onset of IgE elevations. It is suggested that the phenomenon of IgE peaks in the population of patients investigated was due to disturbance of T-cell regulation, i.e. a temporary impairment of T-suppressor cell activity.

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Section: Discussioncontrasting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Transient Elevation of Serum IgE after Allogeneic Bone-Marrow Transplantation

Korver

Schellekens

Dooren

et al. 1987

Int Arch Allergy Immunol

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“…Indeed, a major increase in IgE serum levels has been reported after allogeneic bone marrow transplantation in association with clinical evidence of GVHR (Geha et al, 1980;Saryan et al, 1983;Heyd et al, 1988). This hyper IgE was thought to be due either to a deficiency in IgE-specific suppressor T cells or to activation of IgE-specific T helper cells releasing an IgE-specific inducing factor (Saryan et al, 1983). Because of the similarities between murine and human IgE regulation (Vercelli & Geha, 1989), the hyper IgE observed in human GVH disease could also be related to an enhanced production of …”

Section: Discussionmentioning

confidence: 99%

Hyper IgE in stimulatory graft-versus-hostdisease: role of interleukin-4

Doutrelepont

Moser

Léo

et al. 1991

Clinical and Experimental Immunology

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SUMMARYIntravenous injection of 2 x 108 DBA/2 spleen cells into adult intact (C57BL/6 x DBA/2) Fl mice results in a stimulatory graft-versus-host reaction (GVHR) linked to the recognition by donor CD4+ T cells of Ia alloantigens on host B cells. In the experiments presented here, we found that this GVHR is associated with a major increase in IgE serum levels which was already present 7 days after the cell transfer. At 6 weeks, mean IgE levels were more than 200-fold above the control values. Host B cells were responsible for the hypersecretion of IgE in stimulatory GVHR since it was also observed when the DBA/2 donor inoculum was depleted of B cells but not when the Fl recipients were irradiated. The induction of IgE secretion required donor CD4+ T cells as treatment of the donor inoculum with lytic anti-CD4 monoclonal antibody (MoAb) completely prevented the occurrence of the hyper IgE whereas depletion of CD8 + cells had no influence on this parameter. The role played by interleukin-4 (IL-4) in this model was analysed in vivo by the administration of the I1 B 11 anti-IL-4 rat MoAb (total dose 36 mg) during the first 12 days following induction of stimulatory GVHR by 8 x 107 DBA/2 spleen cells. This treatment completely prevented the development of hyper IgE whereas the administration of a control rat MoAb had no significant effect. We conclude that stimulatory GVHR in mice is associated with a major increase in serum IgE which is mediated by

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“…Human Fc,R+ TCL were established from Fc,R' T cells obtained from patients with the hyper-IgE syndrome. These patients possess extremely high serum IgE levels, their peripheral blood lymphocytes spontaneously secrete large amounts of IgE in vitro and their T cells secrete soluble factors which potentiate IgE production [16][17][18][23][24][25]]. …”

Section: Discussionmentioning

confidence: 99%

Production of IgE‐potentiating factor in man by T cell lines bearing Fc receptors for IgE

1984

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The regulation of human IgE production in vitro by soluble T cell factors was examined. T cells were isolated from the peripheral blood of 2 patients with the hyper-IgE syndrome on the basis of their expression of Fc receptors for human IgE (Fc epsilon R). The T cells were incubated with human myeloma IgE (10 micrograms/ml), washed, reacted with immunosorbent-purified goat anti-human IgE conjugated with fluorescein isothiocyanate, and then separated into Fc epsilon R+ and Fc epsilon R- T cells on the fluorescence-activated cell sorter. Fc epsilon R+ T cells and Fc epsilon R- T cells were propagated in culture using supernatants of phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMC) and irradiated autologous PBMC. Supernatants of Fc epsilon R+ T cell lines but not of Fc epsilon R- T cell lines selectively enhanced IgE synthesis in cultures of B cells obtained from patients with allergic rhinitis but not from normal nonallergic subjects. The surface phenotype of the Fc epsilon R+ T cell line was predominantly T3+, T4+, Ia+ with few (15%) T8+ cells. Two T cell clones were grown from the Fc epsilon R+ T cell line by limiting dilution (0.3 cells/well). These clones possessed the T4+ helper/inducer phenotype and secreted IgE-enhancing factor(s). The IgE-enhancing factor(s) which had affinity for insolubilized human IgE was sensitive to treatment with trypsin and neuraminidase, and had as its target an IgE-bearing B cell. These results suggest that a subset of human T cells bearing an Fc epsilon R secretes an IgE-binding glycoprotein which selectively enhances IgE synthesis by IgE-bearing B cells.

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Regulation of human immunoglobulin E synthesis in acute graft versus host disease.

Cited by 43 publications

References 23 publications

Transient Elevation of Serum IgE after Allogeneic Bone-Marrow Transplantation

Transient Elevation of Serum IgE after Allogeneic Bone-Marrow Transplantation

Hyper IgE in stimulatory graft-versus-hostdisease: role of interleukin-4

Production of IgE‐potentiating factor in man by T cell lines bearing Fc receptors for IgE

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