IgE, T cells and transfer factor in mycosis fungoides.

Zachariae, H; Grunnet, E; Ellegaard, Jørgen; Thestrup‐Pedersen, Kristian

doi:10.1136/bmj.1.6116.854

Cited by 17 publications

(14 citation statements)

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“…Elevated IgE levels have been reported in MF [10] and Hodgkin's disease [1], We have not been able to confirm an increased mean IgE in our patients with MF, but reported elevated values in 4 out of 22 cases [15]. 2 of these patients are included in the present study.…”

Section: Discussionmentioning

confidence: 44%

“…TF has been given as treatment to patients with immunodeficiency diseases [6,9] and has been used to intensify cell-mediated immunity in patients with relative immunological defects, among these, patients suffering from neoplastic disorders [8,12]. We have previously presented our results with TF in mycosis fungoides (MF) [14,16] where induction of cellular immunity seems to be depressed [11] and the number of circulating T lympho cytes lowered [15]. …”

mentioning

confidence: 95%

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Transfer Factor in Mycosis fungoides: Three Years Experience

Zachariae¹,

Ellegaard²,

Grunnet³

et al. 1980

Dermatology

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13 patients with clinically and histologically verified mycosis fungoides were treated with transfer factor as additional therapy to the hitherto conventional treatment after this had failed. After approximately 3 years, complete remission was present in 3 patients, 4 patients were significantly improved and registered as being in partial remission, while the condition was registered as no change in 3 patients. 1 patient was found worse, 1 patient had died after discontinuation of therapy and 1 patient was out of the study. In this case treatment was withdrawn because of the development of contact urticaria to nitrogen mustard, her basic therapy. The number of T lymphocytes, which was low prior to treatment, increased to normal values during the therapeutic period. During the first year a decrease in serum IgE was noted. The results of the clinical evaluation seem to indicate that transfer factor may be of value as an additional therapeutic agent in mycosis fungoides. Controlled investigations are needed and are in progress.

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Section: Discussionmentioning

confidence: 44%

mentioning

confidence: 95%

Transfer Factor in Mycosis fungoides: Three Years Experience

Zachariae¹,

Ellegaard²,

Grunnet³

et al. 1980

Dermatology

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“…Although this has led to recommendations favoring slower infusion rates (as used in our patients), pro longing infusion rates beyond several hours in an ef fort to decrease the risk of leukoagglutination reac tions is not desirable because the therapeutic efficacy is reduced. This is thought to occur because of immunomodulation leading to decreased expression of target antigens on cell surfaces after relatively short exposures to MAb directed against such antigens [27][28][29][30], Similarly, cautious and prolonged incremen tal increases in MAb delivery in an effort to 'desensi tize' a patient to prevent ITAR would not be practical because of this consideration.…”

Section: Discussionmentioning

confidence: 99%

Human IgE, IgG and IgA Antibody Responses to T101, a Murine Monoclonal Antibody against Human Lymphocytes: Implications for Pathogenesis, Risk and Avoidance of Adverse Immunologic Reactions

Dykewicz¹,

Cranberg²,

Patterson³

et al. 1990

Int Arch Allergy Immunol

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To study immune responses that may play a role in immediate-type allergic reactions (ITAR) and serum-sickness-like reactions that have been reported with administration of monoclonal antibodies (MAb), we measured by enzyme-linked immunosorbent assay serum levels of IgE, IgG, and IgA human antimurine antibody (HAMA) to T101, a murine IgG2a antibody that has been used in the treatment of cutaneous T cell lymphoma (CTCL) and chronic lymphocytic leukemia (CLL). None of 8 patients (4 with CLL, 4 CTCL) pretreated with T101 had elevated titers of any HAMA class tested as compared to normal control sera. All CTCL patients who had elevated total serum IgE levels, but normal total serum levels of other antibody classes, had significant rises in IgE, IgG, and IgA HAMA to T101 after intravenous MAb infusion. However, the CLL patients who were hypogammaglobulinemic failed to develop significant rises in HAMA. Three patients (2 CLL, 1 CTCL) had ITAR (e.g., urticaria, angioedema, bronchospasm) associated with infusion of T101; prophylactic medication regimens based upon the control of radiographic contrast media reactions were used with apparent benefit in subsequent infusions in these patients. All 8 patients had negative immediate intradermal skin tests (1 μg/ml) to T101 prior to its infusion. Our data confirm that (1) non-IgE-mediated mechanisms cause ITAR from this MAb, possibly by a mechanism inherent in the action of this MAb against lymphocytes, and (2) that isotypic antibody responses to MAb vary with the type of malignancy being treated. Discussed are clinical implications of these data, including risk of HAM A-mediated adverse reactions, limitations of skin testing and desensitization, and use of prophylactic medication regimens to reduce the risk of ITAR.

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“…At least two antisera were used for each specificity, and for many antigens, three or more sera were available. The following HLA antigens were sought: of the A series, A l, 2, 3, 9, 10 (W25 and W26), 11,28,29 tions from the control group are in the antigens HLA-A1 A2 the 'W19' group and B8 and B12 of the B locus. Only for the antigens of the 'W19' group, in particular W31 and W32 is the deviation from the control population significant.…”

Section: Methodsmentioning

confidence: 99%

Distribution of HLA Antigens in Patients with Mycosis fungoides

Dick¹,

MacKie²

1977

Dermatology

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19 patients with plaque-style mycosis fungoides have undergone determination of HLA antigen distribution. Deviations from the expected distribution frequency occurred with the antigens of the W19 group comprising A29, W30, W31 and W32 and of B8 and Al. The W19 group deviation was statistically significant (χ² = 9.7 p value < 0.005). The significance of this observation in relation to reported immunological abnormalities in mycosis fungoides is discussed.

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IgE, T cells and transfer factor in mycosis fungoides.

Cited by 17 publications

References 1 publication

Transfer Factor in Mycosis fungoides: Three Years Experience

Transfer Factor in Mycosis fungoides: Three Years Experience

Human IgE, IgG and IgA Antibody Responses to T101, a Murine Monoclonal Antibody against Human Lymphocytes: Implications for Pathogenesis, Risk and Avoidance of Adverse Immunologic Reactions

Distribution of HLA Antigens in Patients with Mycosis fungoides

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