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Biomedical subjects

D A Levy

Publications and source records attributed to D A Levy.

At least 91 records · Page 5Linked to original sources
PubMed1977

Failure of the putative IgE pentapeptide to compete with IgE for receptors on basophils and masts cells.

We have examined the claim that a pentapeptide resembling a portion of epsilon-chain of IgE can inhibit allergic reactions by competing with IgE for basophil-mast cell IgE receptors. Four laboratories with expertise in different areas collaborated. The following was found. (1) There was no evidence, by autoradiography, that the pentapeptide could block IgE fixation to basophils or displace IgE from these cells. (2) There was no evidence, by histamine release studies that the pentapeptide could block basophil sensitization or remove IgE from actively sensitized cells. The pentapeptide, also, did not impair antigen-induced histamine release. (3) There was no evidence that the pentapeptide could block the skin test response in Prausnitz-Küstner testing with the antigen injected intradermally or orally administered. Neither the correct pentapeptide sequence from the epsilon-chain nor the Fc" fragment of IgE impaired the P-K test. In each series of experiments, IgE myeloma protein, as a positive control, blocked the allergic response. The failure of the pentapeptide to block these reactions was observed at molar ratios of pentapeptide/IgE of 10(6) to 10(7). Our results, therefore, provide no evidence for competition between the pentapeptide and IgE. Even if there should be some weak affinity between the pentapeptide and IgE receptors on basophils or mast cells this would, by virtue of quantitative considerations, be of no clinical relevance.

Autoradiography↗
PubMed1977

The antigen-induced degranulation of basophil leukocytes from atopic subjects studied by electron microscopy.

Suspensions of washed leukocytes were prepared from the blood of atopic subjects and incubated with diluent, ragweed antigen E or rye grass group I antigen. Histamine release into the suspending medium was measured and directly correlated with changes in the ultrastructure of basophil leukocytes from the same tubes. Incubation of leukocytes with either diluent or an antigen to which the donor was not hypersensitive caused no significant histamine release and the morphology of the basophils was unaltered. By contrast, incubation of leukocytes with an intigen to which the donor was hypersensitive caused substantial histamine release and characteristic morphologic changes in the basophils, many of which underwent exocytotic degranulation. Degranulated human basophils showed the following features: (1) an irregular surface, to which platelets and leukocytes were often adherent; (2) reduction in the number of basophilic granules; (3) residual granular material, both in exocytotic cavities and at the cell surface; (4) coated vesicles and cisternae of smooth endoplasmic reticulum, frequently related to the plasma membrane at sites of exocytosis; (5) thin membrane-bounded granules appeared unaltered; (6) no consistent change was observed in centrioles, microtubules, 90 A filaments, mitochondria, or multivesicular bodies, and degranulated basophils appeared ultrastructurally viable; (7) in reaction cell suspensions, nondegranulated basophils often showed a more active contour than control cells; both reacting but nondegranulated basophils and degranulated basophils sometimes showed localized filamentous webs at their periphery.

Antigens↗
PubMed1975

A genetic-epidemiologic study of chronic obstructive pulmonary disease. I. Study design and preliminary observations.

Although certain environmental agents (e.g., cigarette smoking) are known to be causally related to chronic obstructive pulmonary disease (COPD), differential response to their deleterious effects suggests the importance of constitutional (host) factors. The voluminous literature on the familial occurrence of COPD as well as the association between genetically determined serum alpha 1-antitrypsin (alpha 1-at) deficiency and COPD, however, reveals many aspects yet to be clarified. Studies of alpha 1-at indicate that neither its nature nor its relationship to COPD is simple. Moreover, other familial factors are likely involved. To obtain a better understanding of the etiology and pathogenesis of COPD, both genetic and environmental factors are being examined in a multifaceted investigation. The preliminary observations are summarized. COPD patients have a higher frequency of Pi variant phenotypes than those without lung disease. Among other subjects, both cigarette smoking and Pi variant phenotypes are associated with increased pulmonary function abnormality. Finally, there is familial aggregation of pulmonary impairment that cannot be explained entirely by Pi type or smoking.

ABO Blood-Group System↗
PubMed1974

Chronic obstructive pulmonary disease and alpha-1-antitrypsin (Pi) variation: a family study.

A kindred of a white male proband with alpha1-antitrypsin deficiency, ZZ phenotype, and a severe obstructive ventilatory defect secondary to pulmonary emphysema was studied with regard to alpha1-antitrypsin phenotype, serum trypsin inhibitory capacity (T.I.C.), and pulmonary function. T.I.C.'s and alpha1-antitrypsin phenotypes were consistent with autosomal codominant inheritance. While MZ relatives as well as the proband had pulmonary function abnormalities, the pattern varied within the kindred and abnormalities were observed in some MM relatives also.

Adolescent↗
PubMed1971

Immunologic and cellular changes accompanying the therapy of pollen allergy.

We had found previously that children with ragweed hay fever were somewhat less symptomatic after preseasonal immunization with large doses of ragweed pollen extract than were placebo-treated children. To study further the immunologic changes which accompany immunotherapy, these children were treated again the following year. Each patient served as his own control. Serum blocking (IgG) antibody, measured by inhibition of antigen-induced leukocyte histamine release, was increased 20- to 40-fold after therapy. The anticipated postpollen season increase of serum reaginic (IgE) antibody, measured by passive sensitization of leukocytes from nonallergic donors, was suppressed. Instead, the mean titer was decreased after treatment. Total serum IgE levels, measured by radial radioimmunodiffusion assay, were higher than normal; were correlated with reaginic antibody titers; and also did not increase in the pollen season after treatment. The concentration of both IgE and reaginic antibody was lower in the older children, irrespective of treatment. Leukocyte response to ragweed antigen E and guinea pig anti-IgE antiserum was assessed by means of in vitro histamine release techniques. After treatment, the leukocytes of 21 patients were less sensitive (11 cases), or less reactive (10 cases), to antigen E. Response to anti-IgE antibody also was diminished after treatment. In four cases, neither anti-IgE nor antigen E induced histamine release, although both IgE protein and ragweed-specific IgE antibody were present in the patients' own sera. Clinical improvement was correlated best with decreased leukocyte sensitivity and leukocyte reactivity to ragweed antigen E. It appeared that decreased cell sensitivity was related to lower serum reaginic antibody levels. Decreased cell reactivity, in the presence of both IgE protein and IgE antibody in the serum, may indicate a change in cellular response mechanisms. These studies suggest that clinical improvement following specific immunotherapy must be the result of complex changes in the immunologic and cellular components of allergic disease.

Adolescent↗