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Biomedical subjects

B Golding

Publications and source records attributed to B Golding.

83 records · Page 5Linked to original sources
PubMed1981

Human lymphocytes can generate thymus-independent as well as thymus-dependent anti-hapten plaque-forming cell responses in vitro.

Human lymphocytes from peripheral blood, tonsils, and adenoids produced hapten-specific anti-TNP antibodies after in vitro stimulation with TNP-Ba. This antigen did not appear to behave as a polyclonal activator since TNP-Ba-stimulated cells lysed TNP-conjugated sheep erythrocytes (SRBC) but not unconjugated SRBC or DPPC-conjugated SRBC, whereas cells from PWM-stimulated cultures formed hemolytic plaques with both haptenated and unhaptenated targets. In addition, TNP-Ba generated PFC were inhibitable by soluble hapten (TNP-EACA or TNP-BSA). B cells depleted of T cells (less than 1% E-RFC cells) were able to respond to TNP-Ba but not to PWM or TNP-KLH. When varying ratios of T and B cells were added to cultures the TNP-Ba anti-TNP response was found to have a linear correlation with the number of B cells added (r = 0.987) and was maximal in the absence of added T cells. This was in contrast to the response to TNP-KLH, which required T cells at a particular T:B ratio for optimal induction of anti-TNP PFC. Thus, both T-dependent and T-independent anti-hapten responses could be elicited in human lymphoid cell cultures.

Adenoids↗
PubMed1981

Androgen sensitivity and autoimmune disease. I. Influence of sex and testosterone on the humoral immune response of autoimmune and non-autoimmune mouse strains to sheep erythrocytes.

Pre- and post-puberal NZB, DBA/2 and BALB/c mice showed no sex differences in primary IgM plaque-forming cell responses to sheep erythrocyte immunization. Orchiectomy increased and testosterone implants reduced antibody responses only if followed by sublethal irradiation suggesting that androgens may affect rapidly regenerating stem cells and/or their differentiating progeny. Strain differences in target organ sensitivity to androgen were not observed suggesting that NZB autoimmunity does not arise from a pathologic defect in androgen responsiveness.

Animals↗
PubMed1979

Intravenous immunoglobulin therapy for antibody deficiency.

Twenty patients with antibody deficiency were treated at random with either intramuscular immune serum globulin (ISG) or intravenous modified immune serum globulin (M-ISG). Fourteen patients received of 259 M-ISG infusions during 242 months of treatment. Catastrophic vasomotor reactions were not observed. A single dose of 150 mg/kilo M-ISG increased serum IgG values a mean 248 mg%. Intravenous M-ISG therapy was effective in reducing the incidence of acute infections. Subjects receiving M-ISG developed 0.103 acute infections per month of treatment. Patients injected with ISG had 0.295 acute infections per month of treatment. Seven subjects had separate courses of both intravenous M-ISG and intramuscular ISG. Acute infections per month of treatment for M-ISG and ISG were 0.104 and 0.406, respectively.

Adolescent↗
PubMed1976

Angio-immunoblastic lymphadenopathy. A report of 3 cases.

Angio-immunoblastic lymphadenopathy (AILD) was diagnosed in 3 Black patients, AILD is a non-malignant disorder which resembles a malignant lymphoma clinically and morphologically. It is thought to represent an abnormal response of B lymphocytes to antigenic stimuli which are often therapeutic agents. The disorder usually affects adults of the older age group and the clinical course can be rapidly fatal, particularly if vigorous chemotherapy is given. Of the 3 patients with AILD, 2 died from complicating infections within 6 months after the initial diagnosis. The third patient was completely cured after short courses of prednisone and vincristine. It appears that in some patients the disorder may be completely reversible but whether these patients are at a greater risk of eventually developing a lymphoma is uncertain at the present time, and remains to be ascertained by their long-term follow-up.

Adult↗
PubMed1976

In vitro reversal of cellular unresponsiveness induced by levamisole.

Mononuclear cells from twenty-one patients with depressed cellular reactivity were assessed for the ability to produce leucocyte inhibitory factor (LIF) and to transform after PHA stimulation, in the presence or absence of levamisole. Cells from nineteen patients failed to produce significant lymphokines when stimulated with PHA alone, but after a prior 1-hr levamisole pulse normal amounts of LIF were produced. Unstimulated mononuclear cell supernatants from six patients showed LIF-like activity, which could be abolished or decreased in five of the six when the cells were initially treated with levamisole. Mononuclear cells from seven of twelve patients which failed to incorporate [3H]thymidine after PHA activation, showed an increased response after a 1-hr levamisole pulse. Unstimulated mononuclear supernatants from six patients inhibited the lymphoproliferative response of normal cells to PHA. After treatment with levamisole, however, the suppressive effect of these supernatants was decreased or abolished. In vitro levamisole treatment, therefore, not only restores cellular responsiveness in anergic patients but also restricts the uncontrolled release of inhibitory factors.

Cells, Cultured↗
PubMedDate not supplied

Protection from experimental endotoxemia by a recombinant adeno-associated virus encoding interleukin 10.

BACKGROUND: Interleukin 10 (IL-10) is a homodimeric cytokine that shows considerable clinical promise. Adeno-associated virus (AAV) vectors appear increasingly useful for in vivo gene-transfer applications. METHODS: A recombinant AAV type 2 vector encoding human IL-10 (rAAVhIL10) was constructed by using an adenoviral-free, three-plasmid co-transfection. Cytokine production was measured by using an enzyme-linked immunosorbent assay. Endotoxic shock was induced by lipopolysaccharide (LPS) injection. RESULTS: As media from rAAVhIL10-infected COS cells caused a dose-dependent blockade of IL-12 secretion from spleen cells of IL-10 knockout (KO) mice challenged with Brucella abortus, it was clear that vector-derived hIL-10 was biologically active in vitro. Intravenous or intramuscular administration of relatively modest levels of rAAVhIL10 (10(10) genomes) to IL-10 KO mice resulted in hIL-10 secretion into the bloodstream, which, at 8 weeks, gave median serum levels of 0.9 and 0.45 pg/ml, respectively. Acute endotoxic shock led to a 33% mortality rate, and severe morbidity, in control IL-10 KO mice, whereas no mortality and little morbidity were seen in IL-10 KO mice given rAAVhIL10 7 weeks earlier. CONCLUSIONS: The findings demonstrate that a modest dose of rAAVhIL10 administered in vivo provides long-term protection against LPS-induced endotoxic shock in a murine model. Thus, this vector may be useful for clinical applications requiring sustained IL-10 expression, for example in the treatment of several autoimmune diseases.

Animals↗