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Biomedical subjects

M Ballow

Publications and source records attributed to M Ballow.

At least 91 records · Page 5Linked to original sources
PubMed1978

Diphenylhydantoin interstitial nephritis. Roles of cellular and humoral immunologic injury.

A child with diphenylhydantoin hypersensitivity developed an associated interstitial nephritis. Circulating autoantibody of the IgG class which reacted with normal human tubular basement membrane was linearly deposited along host renal TBM. Cell-mediated immunity to the DPH antigen was also present. In addition, deposits of DPH were demonstrated along the renal TBM. It is suggested that initial alteration of host renal TBM by DPH deposition with secondary immune injury directed at the DPH-TBM antigen may have altered the TBM or uncovered new antigenic sites, rendering it susceptible to further injury on an autoimmune basis.

Autoantibodies↗
PubMed1978

Modulation of mixed lymphocyte culture reactivity following alloimmunization between H-1 (Ag-B)-histocompatible rat strains.

H-1 (Ag-B)-histocompatible rats were cross-immunized to study the effects of presensitization on the mixed lymphocyte culture (MLC) reactivity in normally nonresponsive MLC interactions. Lewis (LEW) rats, H-1 (Ag-B), were given s.c. injections of Fischer (F), H-1 (Ag-B), lymhocytes at weekly intervals for 3 weeks. Immunized LEW (Lew-iF) and F lymphocytes showed increased proliferative responses in MLC after the third immunization. The augmented proliferative responses in the MLC between these H-1 (Ag-B)-histocompatible rat strains following immunization may reflect minor histocompatibility antigenic differences. On the other hand, decreased proliferative responses in MLC between Lew-iF and Ag-B (H-1)-disparate rat strains were demonstrated. Alloimmunization across minor histocompatibility differences led to different types of regulatory effects on the MLC interactions. With low MLC responses, e.g., minor histocompatibility differences, the regulation tends to be positive; whereas for strong MLC responses, e.g., major H-1 (Ag-B) differences, the regulation tends to be negative or suppression.

Animals↗
PubMed1977

Biosynthesis of the third component of complement (C3) in vitro by monocytes from both normal and homozygous C3-deficient humans.

Human monocytes synthesized the third component of complement (C3) up to 5 wk in vitro. Evidence for net C3 synthesis was based on (a) incorporation of 14C-labeled amino acids into C3 protein, (b) indentity of the allotype of C3 produced in vitro with that of the doner's serum C3, even in the presence of carrier C3 protein of a different allotype; (c) correspondence of electrophoretic mobility, size, and subunit structure of C3 protein produced in vitro with serum C3; (d) inhibition of C3 production with cycloheximide. Monocytes from two unrelated C3-deficient patients were studied under conditions that supported C3 synthesis by normal monocytes. Serum from each of the patients contained less than 1% of the normal C3 concentration, buth their monocytes produced C3 at approximately equal to 25% of the normal rate when studied after 2 wk in vitro. The C3 produced in vitro by monocytes from one of the patients had the molecular weight of normal serum C3 and dissociated appropriately under reducing conditions. Monocytes from C3-deficient patients could not be distinguished from normals on the basis of morphology, rosetting with C3-coated erythrocytes, or rates of C2, and total protein synthesis.

Blood Proteins↗
PubMed1975

C1-bypass complement-activation pathway in patients with chronic urticaria and angio-oedema.

During the routine screening of 152 patients with urticaria or angio-oedema for hypocomplementaemia, 4 patients were found to have low serum levels of the third component of complement (C). These patients were noteworthy and differed from previous reports of patients with urticaria-like skin lesions and hypocomplementaemia because of the absence of immune-complex disease. In addition to the low C3, 2 of these patients were unique on the basis of low serum levels of haemolytic C1, C1q, C1s, and properdin factor B, but normal concentrations of C4 and C2. These C abnormalities may reflect a new clinical entity, and these cases form the first description in man of the C1-bypass complement-activation pathway.

Adult↗
PubMed1975

Complete absence of the third component of complement in man.

A 4-yr-old female patient who has recurrent infections with encapsulated bacteria and gramnegative organisms was found to have a complete absence of total hemolytic complement and C3. Total hemolytic complement was reconstituted by the addition of functionally pure C3. With the exception of a moderately reduced homolytic C4, all other C components, measured homolytically and by radial immunodiffusion, were present in normal amounts. By Ouchterlong analysis, the patient's serum contained C3b inactivator and properdin but no antigenic C3. Activation of the alternate pathway was examined by purified cobra venom factor (CVF) and inulin. Neither of these substances led to activation of properdin factor B to B. On addition of partially purified Cordis C3, in four out of four instances and with different preparations of Cordis C3, activation of factor B to B occurred in the inulin-serum-C3 mixture. In contrast, activation of factor B to B occurred only once out of four times with CVF-serum-C3 mixtures. Immune adherence was found to be normal in the patient's serum and could be removed by anti-C4 antiserum of hydrazine treatment. A marked opsonic defect was present against Escherichia coli. Serum bactericidal activity against a rough strain of E. coli was also defective. The ability to mobilize an infalmmatory response was examined by Rebuck skin window technique. A delay in neutrophil migration occurred until the 6th h. In vitro lymphocyte transformation and serum immunoglobulins were normal. The proportion of peripheral blood T cells forming spontaneous sheep erythrocyte rosettes and the percentage of B cells forming EAC rosettes by the C3 receptor were normal. The significance of the absence of C3 in our patient is emphasized by the increased number of infections with encapsulated bacteria and the decreased functional biological activities of the C system, important in host defense mechanism(s).

Blood Bactericidal Activity↗
PubMed1975

Complement in graft versus host disease: IL Depletion of complement components during a systemic graft versus host reaction in the rat (38499).

Serum complement (C) and C components were examined during a systemic graft versus host (GVH) reaction in the rat. In our series of experiments (Lewis times Brown Norway) F-1 hybrid rats (60-80g) were given 200 times 10-6 or 400 times 10-6 Lewis spleen cells intravenously. Clinical GVH disease appeared 5-7 days after cell injection. Five of six rats in the experimental groups had a fall in levels of serum C2 (20-76%) and C4 (75-98%). Only one of six rats in the control group had a significant fall in C components. In a subsequent experiment (Fisher 344 times Brown Norway) F-1hybrid rats (60g) were given 400 times 10-6 Fischer 344 spleen cells or 200 times 10-6 Fischer 344 Ficoll-Hypaque separated spleen lymphocytes. Clincal GVH disease in this instance appeared on day 10. As in the previous experiments C2 and C4 fell markedly, 20-60% and 60-8-%, respectively, from baseline titers. The control groups did not have a significant fall in C2 or C4. Further examination showed reduction in C3, C5, C6,AND C8 suggesting a sequential activation of the C system via the classical pathway. We have postulated that the cells undergoing blast transformation may be activating the C system through membrane changes during the GVH reaction. Furthermore, the deficiency of C AND C components during GVH disease may contribute to the increased susceptibility of the host to infection and sepsis.

Animals↗
PubMed1975

Transfer factor therapy: evidence for nonspecificity.

Four patients were treated with multiple doses of dialyzed transfer factor in which one Wiskott-Aldrich patient with abnormal IgG monocyte receptors obtained benefit. All patients converted skin reactivity, and had improved in vitro lymphocyte responses to varying degrees. Three patients developed positive reactivity to allogeneic cells in MLC, and one patient developed DNCB reactivity. These latter two findings suggest transfer factor may act by inducing a nonspecific maturation of lymphocyte function. A possible mechanism for the action of transfer factor is discussed.

Antibody Formation↗
PubMed1974

Effect of transfer factor therapy on mixed lymphocyte culture reactivity.

We have studied the effect of dialyzable transfer factor therapy on three patients with immunodeficiency disease and in one patient who demonstrated no evidence of deficiency of either humoral or cellular immunity. We found evidence for nonspecificity in the effect of transfer factor on mixed lymphocyte culture reactivity. The data suggest that in patients with immunodeficiency disease a maturation of lymphocytes may lead to a generalized increased immune responsiveness. More profoundly, our data show that transfer factor may induce changes in the expression of histocompatibility determinants. We observed changes in the expression of determinants capable of stimulating in the mixed lymphocyte culture reaction as well as an increase in the capacity of lymphocytes to respond.

Antigens, Bacterial↗