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Biomedical subjects

M Ballow

Publications and source records attributed to M Ballow.

At least 55 records · Page 3Linked to original sources
PubMed1982

Familial chronic mononucleosis.

A syndrome of chronic mononucleosis occurred in two members of a family. Symptoms were chronic malaise and fatigue; recurrent upper respiratory tract infections; and mild, variable immune abnormalities. Intermittently positive heterophil titers were present for more than 2 years after acute infectious mononucleosis. Epstein-Barr-virus-specific antibodies were persistently abnormal. In the proband, the R component of the early antigen complex was present for 3 years and she never developed normal antibodies to Epstein-Barr nuclear antigen. Her brother had low to absent Epstein-Barr nuclear antigen titers, and antibodies to both the R and D component of the early antigen complex. Primary and acquired immunodeficiency states can show abnormal Epstein-Barr-virus-specific serologic findings that may reflect an attempt by the host to limit virus spread in the presence of deficient immune responses. This action may result in alterations of the Epstein-Barr virus-latent state, and lead to a chronic active infection and a syndrome of chronic mononucleosis.

Adult↗
PubMed1982

Abnormal anti-Epstein Barr virus antibodies in carriers of the X-linked lymphoproliferative syndrome and in females at risk.

The asymptomatic hemizygous female carriers of the X-linked lymphoproliferative syndrome (XLP) have abnormal antibody responses to EBV. This suggests partial expression of the defect that leads to EBV-provoked life-threatening diseases in their affected sons. EBV specific antibodies were measured in 65 serum samples of 12 obligate carrier females and seven of their daughters (females at risk) during periods ranging from 1 to 5 yr. Abnormal qualitative antiviral capsid antigen (VCA) IgG titers were nearly fourfold higher than normal controls, two carriers had persistent IgM anti-VCA antibody, two-thirds had persistent IgA anti-VCA antibody, and half of the women had titers to early antigen (EA). Five of seven females exhibited a similar persistent pattern. In contrast, none of the unaffected family members nor 23 normal controls expressed IgA or IgM titers to VCA even with high exposure to the virus, and anti-EA was detected in only one control. Therefore, these findings may prove useful for detecting carriers of the syndrome. Abnormal anti-EBV titers similar to the carrier pattern have been reported in patients and other immunosuppressed individuals, and are indicative of active viral infection.

Adolescent↗
PubMed1982

Immune deficiency in the X-linked lymphoproliferative syndrome. II. Immunoregulatory T cell defects.

Surface phenotypic markers and the function of lymphocytes in patients affected with the X-linked lymphoproliferative syndrome (XLP) were studied. This syndrome is characterized by a defective response to infection with Epstein Barr virus (EBV). Normal numbers of B and T cells were detected with anti-Ig and monoclonal OKT3 antisera, respectively. T cell subset values, however, were persistently altered: cells reacting with OKT8 were significantly elevated in five of nine patients, accompanied by a slight decrease in the percentage of OKT4-positive cells, leading to abnormally low OKT4 to OKT8 ratios. One patient had a high OKT4 to OKT8 ratio due to low number of OKT8-positive cells. Lymphocytes from patients showed normal proliferation after stimulation with T and B cell mitogens. In contrast, Ig synthesis by lymphocytes after stimulation with B cell mitogens was markedly deficient: low or undetectable levels of one or all classes of Ig were detected, whereas cell lines established from EBV-infected B lymphocytes from patients produced normal quantities of Ig. These studies imply immune regulatory impairments in the patient with XLP.

Antibodies, Monoclonal↗
PubMed1981

Pemphigus-like mucosal lesions: a side effect of penicillamine therapy.

A patient with Wilson's disease on long-term penicillamine therapy was seen for evaluation and management of chronic persistent debilitating stomatitis, which was subsequently determined to be cytologically and histologically consistent with pemphigus vulgaris. A brief review of the pertinent literature disclosed that the dermatologic lesions of pemphigus secondary to penicillamine are alleviated by discontinuation of penicillamine and institution of prednisone therapy. Our patient's primarily oral lesions did not resolve with this recommended alteration in therapy, since penicillamine could be discontinued only briefly in the interest of maintaining acceptable serum copper levels and because of the paucity of available alternative copper-chelating agents. Eventually the patient was placed on tetraethylene tetramine (TETA), an experimental copper-chelating agent, and betamethasone (Celestone). This has provided a satisfactory reduction in serum copper levels and resolution of the oral lesions.

Adult↗
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↗