The use of transfer factor in a patient with agammaglobulinemia.

We have studied a 9-year-old boy with agammaglobulinemia treated for the past 6 years with exogenous gamma-globulin who was noted to have an immunoglobulin (Ig)M level of 35 mg/100 ml and circulating B cells as determined by immunofluorescence. Of the circulating lymphocytes, 41% had alpha-immunoglobulin heavy chains, 3% gamma chains, and 3% mu chains. Synthesis of gamma heavy chain classes showing wide heterogeneity and alpha and mu chains of restricted mobility was demonstrated by radioimmunoelectrophoresis. Because of the patient's poor clinical response to exogenous gamma-globulin administration and the paradoxic presence of circulating B cells, with the capacity to synthesize immunoglobulins in vitro, we elected to begin a course of therapy with transfer factor. After the initial four doses of transfer factor (2 x 10(8) lymphocytes/dose) his serum IgG rose from 50 to 130 mg/100 ml, the same level which he had previously attained during continuous exogenous gamma-globulin therapy. His serum IgG has remained at this level for the past 12 months with trimonthly booster doses of transfer factor. The patient has not required any additional gamma-globulin therapy and he has remained clinically asymptomatic. Our studies in a patient with agammaglobulinemia have shown that transfer factor therapy may affect immunoglobulin synthesis. The concurrent discontinuation of exogenous gamma-globulin administration makes it difficult to attribute the changes to only one or another aspect of therapy. We await further reports of the effects of transfer factor in the therapy of patients with B cell disorders.

Intracellular localization of the migration inhibitory factor (MIF) in a long-term human lymphoid cell line.

Subcellular fractions of the human lymphoid cell line PGLC-33H were obtained by N2 cavitation and differential centrifugation. The purity of the fractions was assessed by the use of the following marker enzymes: beta-glucuronidase for the lysosomal-intermediate fraction; a nonspecific esterase for the microsomal fraction; and LDH for the supernatant fraction. These subcellular fractions were studied for MIF activity utilizing human lymphoid cells from established lines as target cells. MIF activity was most consistently found in the microsomal fraction. Also, MIF activity was closely associated with the relative specific activity of exterase. No such correlation with MIF activity could be demonstrated for beta-glucuronidase or LDH.

Host responses to Epstein-Barr virus and cytomegalovirus infection in leprosy.

A study was undertaken in patients with leprosy to assess the contribution of cell-mediated immunity to the host response to Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infection. Sixteen of 72 patients (22%) with lepromatous leprosy, with impaired cellular immunity, had anti-EBV titers of 1,640 or higher. Only 4 of 49 patients (8%) with tuberculoid leprosy, with intact cell-mediated immunity, attained the level of 1:640. The anti-EBV antibody titers were significantly higher in patients with lepromatous leprosy (P approximately 0.025). No significant differences were found in the level of anti-CMV antibody titers in patients with the two types of leprosy. The presence of high anti-EBV antibody titers in lepromatous leprosy suggests that cell-mediated immunity is a significant factor in host response to EBV infection. Host immune responses should be taken into consideration when assignment of an etiological role to EBV is based upon seroepidemiological data.