Transfer Factor Therapy Research Articles

Transfer Factor Revisited: Treatment of Congenital Cytomegalovirus Infection

A 7-month-old girl with congenital cytomegalovirus (CMV) infection underwent an immune assessment in anticipation of Transfer Factor therapy. She had been symptomatic since birth, with jaundice, rhinorrhea, diarrhea, pneumonia, hepatosplenomegaly, chorioretinitis, hydrocephalus (for which she was shunted), motor retardation, and failure to thrive. Her sputum and urine cultures were positive for CMV and her IgM anti-CMV antibody titer was positive at 1:16-1:32 dilutions. Her baseline immune assessment was normal except for a failure of her peripheral blood mononuclear cells to produce migratory inhibitory factor in response to CMV antigen. Treatment with transfer factor prepared from CMV seropositive donors resulted in clinical improvement, clearance of the virus, normal migratory inhibition factor responses to CMV antigen, and subsequent development of normal growth and development parameters.

Lymphocyte transfer factor therapy in malnutrition and infection.

Journal Article Lymphocyte Transfer Factor Therapy in Malnutrition and Infection Get access Nutrition Reviews, Volume 35, Issue 5, May 1977, Pages 102–104, https://doi.org/10.1111/j.1753-4887.1977.tb06556.x Published: 01 May 1977

Treatment of cryptosporidiosis with oral bovine transfer factor

Cryptosporidia are intestinal protozoans long known to cause diarrhea in humans, especially those with acquired immune deficiency syndrome (AIDS). When transfer factor prepared from calves which possessed delayed-type hypersensitivity to Eimeria bovis was given to nonimmune calves and mice it conferred protection against clinical infection (coccidiosis). Recent studies with oral bovine transfer factor have shown that it can confer cell-mediated immunity to humans. Based on these findings we decided to treat eight AIDS patients suffering from Cryptosporidium-associated diarrhea with transfer factor prepared from calves immune to Cryptosporidium- Prior to treatment with transfer factor, three patients had been treated with spiramycin, one patient with α-difluoromethylornithine (DFMO), and one patient with furazolidone for greater than 1 month without clinical or laboratory improvement. Following administration of transfer factor, five or eight patients exhibited a decrease in the number of bowel movements and the development of formed stools. Cryptosporidium was eradicated from the stools of four patients but two of these patients subsequently relapsed and one patient continued to have diarrhea despite the absence of Cryptosporidium in the stool. One patient has been free of diarrhea and Cryptosporidium for 2 years after discontinuation of transfer factor therapy.

Augmentation of skin test reactivity and lymphocyte blastogenesis in patients with AIDS treated with transfer factor

Nine patients with the acquired immunodeficiency syndrome (AIDS) were administered four doses of pooled transfer factor obtained from the lymphocytes of three healthy controls and three homosexuals with stable lymphadenopathy and serum antibody to the human immunodeficiency virus. Before receiving transfer factor, all patients exhibited anergy to skin test antigens. After four weeks of transfer factor therapy, six of seven patients tested had at least one skin test response. Lymphocyte blastogenic responses to phytohemagglutinin rose from a stimulation index of 6.77 +/- 1.31 before treatment to 19.77 +/- 6.24 after four weeks of transfer factor therapy. Smaller but significant increases were also seen in blastogenic responses to antigens. Improvements in immune responses diminished after administration of transfer factor was halted. Thus, administration of transfer factor to patients with AIDS resulted in partial immune reconstitution. Further studies are indicated to examine the clinical efficacy of this immune response modifier in the treatment of AIDS.

Augmentation of Skin Test Reactivity and Lymphocyte Blastogenesis in Patients With AIDS Treated With Transfer Factor

Nine patients with the acquired immunodeficiency syndrome (AIDS) were administered four doses of pooled transfer factor obtained from the lymphocytes of three healthy controls and three homosexuals with stable lymphadenopathy and serum antibody to the human immunodeficiency virus. Before receiving transfer factor, all patients exhibited anergy to skin test antigens. After four weeks of transfer factor therapy, six of seven patients tested had at least one skin test response. Lymphocyte blastogenic responses to phytohemagglutinin rose from a stimulation index of 6.77 +/- 1.31 before treatment to 19.77 +/- 6.24 after four weeks of transfer factor therapy. Smaller but significant increases were also seen in blastogenic responses to antigens. Improvements in immune responses diminished after administration of transfer factor was halted. Thus, administration of transfer factor to patients with AIDS resulted in partial immune reconstitution. Further studies are indicated to examine the clinical efficacy of this immune response modifier in the treatment of AIDS.

Transient recovery of serum IgG level by transfer factor in a case of dysgammaglobulinemia

Dysgammaglobulinemia type 1 is one of congenital immunodeficiency syndromes which is characterized by higher or normal serum IgM level and deficiency of IgG and IgA.Recently we encountered a one-year-old boy who had recurrent respiratory infections and lymphadenitis; IgG and IgA levels in his serum were extremely low in spite of the upper limit of normal range of serum IgM level. Salivary IgA was also deficient. The percentage of EAC-rosette forming cells and surface IgA bearing lymphocytes was lowered. Delayed hypersensitivity skin tests with PHA, PPD and candida antigens were normal. lymphocyte stimulations induced by the mitogens, PHA and pokeweed were also normal.Treatment of this patient was started with intravenous administration of sulfonated γ-globulin. With this therapy serum IgM level was gradually decreased. γ-globulin replacement therapy was repeated every three or four weeks. As the patient was suffered from interstitial pneumonitis, transfer factor (1 unit/week, 4 units) therapy was also started. During transfer factor therapy the serum IgG levels of this patient was kept at the normal range for three months without γ-globulin replacement therapy.Although the mechanism of transient recovery of serum IgG level by transfer factor is not clear, we suspect that the switch from IgM to IgG synthesis may have been accomplished by a nonspecific facilitation by transfer factor of T-B cell interaction in our patient.

Transfer factor and repeated otitis media

The effect of transfer factor (TF) was investigated in 12 children with repeated otitis media. These patients were immunologically compared to a control group of 23 age-matched healthy children. Levels of immunoglobulins, total and “active” T-cells, and phagocytic activity of granulocytes and monocytes were evaluated in the 12 children prior to, during, and after TF therapy. Percentages of “active” T cells and absolute numbers of “active” T and total T cells, which were initially low in the patient group, increased significantly after TF therapy to statistically match those of the healthy control group. The percentage of phagocytic monocytes in patients after therapy did not differ from healthy children; however, the percentage of phagocytic granulocytes remained depressed significantly. The levels of IgG, IgA, and IgM were unaffected by the therapy although the IgA and IgM were higher in the patient population throughout the study. After therapy, one-half of the patient population remained asymptomatic for a 1-year period and the others had markedly reduced attack rates.

Is controversy about ‘transfer factor therapy’ nearing an end?

Nearly 30-years after Lawrencefirst described ‘transfer factor’ the therapeutic value of dialysable leukocyte extracts is now being examined in adequately designed trials. The evidence of its efficacy in certain patients in certain circumstances is unmistakable.

Recovery of neutrophil functions by transfer factor therapy in Wiskott-Aldrich syndrome

Recovery of neutrophil functions by transfer factor therapy in Wiskott-Aldrich syndrome

Transfer Factor Therapy in Patients with HBs Ag Positive Chronic Hepatitis

Transfer Factor Therapy in Patients with HBs Ag Positive Chronic Hepatitis

Transfer factor therapy for histoplasmosis in a patient with Hodgkin's disease

Transfer factor therapy for histoplasmosis in a patient with Hodgkin's disease

Transfer Factor Therapy for Histoplasmosis in a Patient With Hodgkin's Disease

A patient with recurrent chronic histoplasmosis was diagnosed also as having Hodgkin's disease. Studies of cell-mediated immunity (CMI) demonstrated no reaction to histoplasmin by skin test, lymphocyte transformation (LT), or leukocyte inhibition factor (LIF) assay. Clinical and immunologic studies were performed during treatment with 19 doses of dialyzable transfer factor (TF) prepared from a normal donor with strong CMI against histoplasmin. Transfer of CMI to the patient was demonstrated by all three tests. All tests reverted to nonreactive during the period of observation. Repeated doses of dialyzable TF were followed by reconversion of skin tests. The LIF assay was most reactive. Reactivation of histoplasmosis occurred during antimetabolic therapy for Hodgkin's disease; however, the lesions cleared rapidly when TF was added to amphotericin B. Amphotericin B was administered at a dosage of 25 mg three times each week during the entire study.

Nephropathy in the Wiskott-Aldrich Syndrome

Nephropathy was detected in five of 32 patients with the Wiskott-Aldrich syndrome who were participating in a study of transfer factor (TF) therapy. In two patients, nephropathy was present before TF and did not appear changed by TF therapy. One of these patients subsequently developed progressive renal failure requiring dialysis beginning 5 1/2 years after TF therapy. In two patients, decreased renal function appeared very soon after the administration of TF. One patient showed gradually decreasing renal function beginning after two years of TF therapy. An additional patient was identified who died with renal failure without having received TF. The results suggest that renal failure occurs in the Wiskott-Aldrich syndrome more frequently than generally recognized and that administration of TF may precipitate or accelerate the renal disease in patients with this syndrome.

Transfer factor therapy in psoriasis.

Recent investigations suggested a mild defect in cell-mediated immunity in patients with psoriasis vulgaris [1]. It is not dear, however, whether these findings are of pathogenetic importance or solely represent epiphenomena of a chronic inflammatory disorder. Transfer factor therapy can restore cellular immunity in certain pathological conditions [2]. Thus, a clinical pilot study of this preparation seemed justified in psoriasis. Transfer-Faktor human (polyvalent), Fa. Schura Blutderivate, Krefeld, FRG, was used in this study (we thank Dr. Baginski for providing the preparation). It consists of deoxyribonuclease-treated, dialyzed lysates of pooled leucocytes from at least 10,000 human blood donors in a lyophilized form. The reconstituted solution represents 5 • 10 l~ leucocytes/100 ml. Dosage: Day 1: I ml/kg body weight. Day 4: 2 ml/kg. Day 8 : 3 ml/kg intravenously. Four patients were included in this pilot study:

Chemoimmunotherapy of disseminated malignant melanoma with DTIC-BCG, transfer factor + melphalan.

The experimental synergism of melphalan with DTIC and the ability of transfer factor to improve immunocompetence were the basis of an attempt to improve therapeutic results in disseminated malignant melanoma. Sixty-four evaluable patients with disseminated malignant melanoma were treated in a 21-day cycle as follows: DTIC 250 mg/M2 intravenously days 1 to 5, Connaught BCG 6 X 10(8) organisms on days 7, 12, and 17 by scarification, and transfer factor 1 unit (10(9) lymphocytes equivalent, from immunocompetent relatives of patients) subcutaneously on day 12, with or without L-PAM 30 mg/M2 on day 1. Twenty-nine patients received L-PAM and 35 did not. Remission rates of 17% and 23%, respectively, occurred in these groups. An additional 15 patients received DTIC-BCG and three doses of transfer factor on days 7, 12, and 17 and had a remission rate of 20%. Remission duration and survival were compared to historical controls of 111 patients treated with DTIC and 89 treated with DTIC-BCG. Median survival on DTIC-BCG-Transfer Factor was seven months compared to four months for DTIC (P = .003) but did not differ from DTIC-BCG. Addition of L-PAM did not improve remission duration or survival compared to DTIC-BCG but enhanced myelosuppression and immunosuppression. A 60% increase in delayed type hypersensitivity to recall antigens occurred in this study compared to 34% with DTIC-BCG (P = .005). Prognosis and immunocompetence were not directly related. In summary, in this study, (1) transfer factor therapy did not enhance the clinical effects of DTIC-BCG, although it augmented delayed type hypersensitivity to recall antigens; and (2) L-PAM was not additive to DTIC in the treatment of disseminated malignant melanoma and may have abrogated the effect of immunotherapy.

Immunocompetence and transfer factor therapy in uveitis.

A study of the clinical course of 20 patients with uveitis treated with transfer factor is reported. Twelve (60%) of the patients were initially immunoincompetent on screening. Eight of the 12 changed to an immunocompetent status after treatment and could either decrease or discontinue their anti-inflammatory drugs. Five had a statistically significant improvement in visual acuity. One of the 8 initially immunocompetent patients had a statistically significant visual improvement, and 2 decreased or discontinued all drugs, while 3 increased their drugs.

Immunotherapy of osteogenic sarcoma with transfer factor

Fifteen patients with osteogenic sarcoma were treated with transfer factor derived from leukocytes of their household contacts. Eight of the fifteen patients were tumor-bearing, and transfer factor therapy was correlated with increased cell-mediated immunity in peripheral blood lymphocytes and with lymphocytic infiltrates into the tumors. There was no marked increased in survival time as compared with historical controls, but this therapy did not accelerate the disease, and there were no untoward side effects.

Immunologic reconstitution, autoimmunity, and T-cell immune deficiencies

A 17-month-old female with combined immunodeficiency, a proliferative response to allogeneic cells in MLC, and circulating B lymphocytes (50%, all with surface immunoglobulin M) was treated with transfer factor (TF). After six doses of transfer factor, serum levels of IgG increased from 234 mg/dl to 1071 mg/dl and a lymphocyte proliferative response was detected to pokeweed mitogen. However, no change in T-cell function was observed. Clinically, she did well, but after the eighth dose of transfer factor, she developed the nephrotic syndrome. Renal biopsy suggested immune complex glomerulonephritis. Subsequently following treatment for Pneumocystis carinii, a 20-day cultured thymus was transplanted intraperitoneally. Two weeks after thymus transplant, the patient started to develop delayed skin reactivity and in vitro mitogen responsiveness. Six weeks posttransplant, the PHA and pokeweed mitogen responses were approximately 60% of normal, but the Concanavalin A response had disappeared. Subsequently she developed a Coombs positive hemolytic anemia, a cutaneous vasculitis, and thrombocytopenia. There was no evidence of GVH disease. Multiple autoimmune manifestations developed in association with transfer factor therapy and transplantation of cultured thymus tissue. T-Cell deficiencies are predisposed to autoimmune diseases because of imbalances of regulatory T-cell function. These imbalances of regulatory T-cell function may occur especially following partial immune reconstitution. The changes in B-cell function during transfer factor therapy may have resulted from enhanced T-cell-B-cell interaction. This immunopotentiation effect of transfer factor together with partial T-cell reconstitution may have led to B-cell hyperresponsiveness and autoimmune disease.

Transfer factor therapy in the Wiskott-Aldrich syndrome. Results of longterm follow-up in 32 patients : Spitler LE: Am J Med 67: 59–66, 1979

Transfer factor therapy in the Wiskott-Aldrich syndrome. Results of longterm follow-up in 32 patients : Spitler LE: Am J Med 67: 59–66, 1979

Transfer factor therapy in the Wiskott-Aldrich syndrome: Results of long-term follow-up in 32 patients

Thirty-two patients with the Wiskott-Aldrich syndrome have been treated with transfer factor provided by this laboratory. Apparent clinical benefit was observed in 44 per cent of them. The mean age of the patients who showed clinical benefit was significantly greater than that of the patients who showed no benefit. Conversion of immunologic reactivity correlated with clinical benefit. Thirteen of the patients who received transfer factor are alive, and 17 have died (43 per cent survival). Clinical benefit was correlated with survival. The median survival was greater than five years in the patients who showed clinical benefit, whereas it was 18 months in those who did not show clinical benefit. We conclude that transfer factor caused conversion of immunologic parameters, apparent clinical benefit and prolonged survival in some, but not all, patients with the Wiskott-Aldrich syndrome.