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Biomedical subjects

I L Strannegård

Publications and source records attributed to I L Strannegård.

11 recordsLinked to original sources
PubMed1992

Pityrosporum ovale and atopic dermatitis in children and young adults.

Children aged 0-21 years, 60 children with atopic dermatitis (AD), 40 children with rhinoconjunctivitis and or asthma (RA) and 40 children with no atopic history (HC) were studied to evaluate the relationship between skin colonisation with Pityrosporum ovale and the occurrence of specific IgE antibodies to P. ovale. The following studies were done: culture for P. ovale, measurement of IgE antibodies to P. ovale (skin prick test, RAST), Candida albicans, and Cladosporium herbarum (RAST) and IgG antibodies to P. ovale. P. ovale could be cultured with about the same frequency in children and young adults with AD and age-matched children with or without other atopic manifestations. In spite of similar colonisation, IgE antibodies against P. ovale occur only in atopy and more frequently in children with AD than in those with other types of atopic disease.

Adolescent↗
PubMed1979

Stimulatory and inhibitory effects of cyclic AMP on lymphocytes from atopic children.

The effect of cholera toxin and dibutyryl cAMP on mitogen-activated lymphocytes from atopic and non-atopic individuals was studied. Cholera toxin enhanced stimulation by phytohemagglutinin of cells from small children but not from adults. Dibutyryl cAMP at low concentration (less than 10(-5) M) significantly enhanced the lymphocyte response to mitogens in some, but not all individuals. High concentrations, on the other hand, were consistently inhibitory. In atopic children, the lymphocyte response to T cell mitogen was significantly less stimulated by cholera toxin, and more inhibited by dibutyryl cAMP than the response of cells from non-atopic matched controls. Thus, T cells from atopic individuals appear to have an altered sensitivity to the action of cAMP, possibly resulting in an impaired balance between helper and suppressor T cells. The hypothesis is advanced, that such an altered balance is causally related to hyperproduction of IgE resulting in atopic disease.

Adolescent↗
PubMed1979

Lymphocyte stimulation with phorbol myristate acetate in atopic and non-atopic individuals.

Phorbol myristate acetate (PMA) was found to be a potent stimulator of DNA synthesis in human whole blood cell cultures. Stimulation with pokeweed mitogen was strongly enhanced by addition of PMA-activated cells. PMA responsiveness varied with age, being low or absent in newborns and very pronounced in adults. In atopic children, PMA responsiveness was normal or increased. The ratio of phytohemagglutinin to PMA responsiveness was significantly reduced in cultures from such children. This finding would be compatible with the hypothesis of a relative suppressor cell deficiency in atopic disease. The results of tests designed to detect suppressor and helper cell activity, added further support to this hypothesis.

Adolescent↗
PubMed1979

In vitro differences between the lymphocytes of normal subjects and atopics.

Recently evidence has accumulated that atopic disease is associated with a deficiency of thymus-derived (T) cells. This deficiency appears to be primary, rather than secondary to treatment or manifestations of the disease. Results of in vitro studies indicate that the deficiency is most pronounced in certain subpopulations of T cells, and therefore a disturbance of the balance between subsets of T cells, notably suppressor and helper T cells, may develop in vivo in atopics. Some results suggest that there is indeed a relative deficiency of suppressor T cells in atopic diseases, and thus the hyperproduction of IgE which is associated with these diseases may be explained. The cause of the T cell deficiency in atopy may be a basal cellular abnormality, manifested e.g. as increased sensitivity to inactivation by physiological substances, notably to agents which increase intracellular levels of cyclic AMP. It is equally possible that the T cell deficiency is a direct consequence of subnormal production of certain thymic hormones.

Animals↗
PubMed1977

Increased sensitivity of lymphocytes from atopic individuals to histamine-induced suppression.

Histamine depressed lymphocyte reactivity to phytohemagglutinin and, to a lesser degree, concanavalin A, when administered simultaneously with mitogen to lymphocyte cultures. Addition of histamine at later times to the cultures appeared to have a slightly enhancing effect on the lymphocyte response. Stimulation of lymphocytes with pokeweed mitogen was in some cases enhanced, even by high concentrations of histamine. Lymphocytes from atopic individuals were more sensitive to the inhibitory effect of histamine than lymphocytes from nonatopic individuals. The sensitivity appeared age-dependent, but within each age group histamine evoked significantly more suppression on lymphocytes from atopic than from nonatopic individuals. The possibility that the altered reactivity of lymphocytes to histamine, which appears to be associated with atopic allergy, is of pathogenic importance, is discussed, and a hypothesis for the development of atopic disease is proposed.

Concanavalin A↗
PubMed1977

Influence of serum from atopic children on T lymphocytes.

The relative and absolute number of peripheral T cells was found to be depressed in atopic children. Sera from atopic children had slightly less stimulatory effects on lymphocyte DNA synthesis induced by PHA, Con A and PPD, than sera from nonatopic children. This finding indicates an occurrence of inhibitory factor(s) in atopic serum. Sera from some severely ill atopic patients almost completely abolished mitogen-induced lymphocyte DNA synthesis. Inhibition by atopic serum appeared to be an early event in lymphocyte mitogenesis and not due to CRP, IgE or factors binding to mitogens. Lymphocytes from atopic children were no more sensitive to suppressive influences of atopic serum factors than were lymphocytes from adult blood donors. Normal serum enhanced mitogen-induced DNA synthesis more in lymphocytes from adult blood donors than in those from atopic children. The results indicate that, although the T cell defect in atopy may be partly caused by serum factors, occurring during clinical allergic disease, the main reason for the defect is probably an altered reactivity of the T lymphocytes in atopic individuals.

Adolescent↗
PubMed1976

T lymphocytes in atopic children.

The number of circulating T and B cells and the sensitivity of lymphocytes to stimulation with phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweek mitogen (PWM) was studied in 233 atopic children. The number of T lymphocytes was found to be decreased in cases of rhinoconjunctivitis, asthma as well as atopic eczema. Levels of B lymphocytes were normal. Sensitivity to stimulation with PHA and to a lesser degree, Con A, was significantly decreased whereas stimulation with PWM was unaffected. The severity of the atopic eczema was inversely correlated to T cell numbers. Several lines of evidence indicated that the abnormalities observed were intrinsically associated with the atopic conditions and not evoked by corticosteroid treatment. The results are compatible with the hypothesis that atopy is associated with a defect of a subpopulation of T cells. The possibility that this subpopulation has a suppressor function on reagin formation is discussed.

Adolescent↗