Cytotoxic Antibody for Epithelial Cells in Human Graft versus Host Disease

Merritt, C. B.; Mann, Dean L.; Rogentine, G. Nicholas

doi:10.1038/232638a0

Cited by 23 publications

(2 citation statements)

References 5 publications

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“…Whether this B-cell response is a secondary effect, following changes in regulatory T-cells following acute GVHD, or whether it is a reflection of B-cell agression taking an active part in cell destruction remains unclear. That B-cells also take part in GVHD is suggested by the description of a cytotoxic IgMantibody against epithelial cell lines in three BMT patients (Merritt et al 1971) and the fmding of dermo-epidermal IgM-deposits in the acute or chronic forms of this disease (Tsoi et al 1978).…”

Section: A Transient Marked Increase In Igg Secretion In Vtfro Duringmentioning

confidence: 99%

Are Increased IgE‐Levels a Signal of an Acute Graft‐Versus‐Host Reaction?

Ringdén¹,

Persson²,

Johansson³

1983

Immunological Reviews

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IgE-levels are markedly elevated following bone-marrow transplantation in patients with and without GVHD. In patients with GVHD, there is a significant correlation between the timing of the IgE-increase and the appearance of clinical GVHD (p less than 0.01). The highest IgE-level (8000 kU/l) was noted in a recipient of a syngeneic graft. During the IgE-peak, the serum from this patient contained low concentrations of IgE reacting with several tested allergens as well as for the hapten TNP, which indicated polyclonal activation. In a patient with a known allergy to animal danders, RAST tests were positive against dog and cat both before and six weeks after total body irradiation and transplantation with marrow from a non-allergic donor. A slight increase in the amount of allergen-specific, IgE-antibodies was seen during the increase in total IgE. A non-allergic patient was transplanted with marrow from a donor allergic to timothy. Timothy-specific, IgE-antibodies were detected immediately after transplantation but they disappeared within a few days and could not be detected during the period of increase in total IgE. We believe that the IgE-elevation seen after conditioning with cytotoxic drugs and total body irradiation in BMT-patients is a polyclonal response in host B-cells induced during an acute, GVHR and influenced by disturbed regulatory T-cells. Lymphocytes from patients with acute GVHD had unusually large numbers of IgG/PFC in vitro after stimulation with staph. aureus Cowan 1 (p less than 0.001), which may reflect a clonal expansion of responsive B-cells.

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Section: A Transient Marked Increase In Igg Secretion In Vtfro Duringmentioning

confidence: 99%

Are Increased IgE‐Levels a Signal of an Acute Graft‐Versus‐Host Reaction?

Ringdén¹,

Persson²,

Johansson³

1983

Immunological Reviews

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“…Recent studies in canine irradiation chimeras (Hellstrom et al 1970) and in three successfully reconstituted patients with CID (Jose et al 1971) have shown that peripheral blood leukocytes were cytotoxic for the fibroblasts of the host, but that this cellular cytotoxicity could be inhibited by an autologous serum factor. On the other hand, four leukemic patients receiving HL-A identical bone-marrow grafts developed a factor cytotoxic for epithelia1 cells but not for lymphoid cells (Merrit et al 1971).…”

Section: Discussionmentioning

confidence: 92%

Studies Non on HL‐A Cytotoxic and Blocking Factor in a Patient with Immunological Deficiency Successfully Reconstituted by Bone Marrow Transplantation

Jeannet

Rubinstein

Pelet³

1973

Tissue Antigens

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The serum of a 12‐year‐old boy with CID, reconstituted by a bone marrow graft from an HL–A identical sibling, was studied for the presence of blocking and cytotoxic antibodies. After grafting, the patient's serum inhibited the response of autologous and of normal lymphocytes in the MLC. A non‐HL–A lymphocytotoxic antibody was detected at the time severe GVHR. It reacted with lymphocytes from the patient's father, mother, sisters, and with 70 % of unrelated allogeneic lymphocytes. It was not reactive with the donor lymphocytes, suggesting that it was formed against a non‐HL–A antigen present on the recipient tissues but absent on the donor cells. Prolonged bone‐marrow allograft tolerance may depend upon active inhibition mediated by a humoral factor.

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