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Biomedical subjects

J L Subiza

Publications and source records attributed to J L Subiza.

43 records · Page 3Linked to original sources
PubMed1987

IgM response and resistance to ascites tumor growth.

Antibody response and protection against Ehrlich ascites tumor (EAT) was studied in eight EAT-immunized strains of mice (AL/N, BALB/C, C57BL/6J, F1 (C57BL/6 x BALB/C), C57BL/10J, B10.BR, CBA/Ca, SW). The results showed a close association between IgM response and resistance to subsequent tumor challenge. Thus, protection was only achieved in those animals giving a measurable IgM response against EAT cell surface antigens, i.e., all inbred strains of mice tested, except CBA/Ca, and some outbred SW mice. The lack of IgM response to these antigens in CBA/Ca was not linked to the strain H-2 haplotype. Resistance could be passively transferred to nonimmunized mice by means of serum, or purified IgM, from protected immune animals. Moreover, complement depletion by cobra venom factor treatment did not modify the protection afforded to those mice. IgM reactivity to EAT cells was completely abolished by previous cell trypsinization. Trypsin removed but did not destroy the antigen(s) recognized by the IgM, since all its activity could be absorbed with the supernatant of the EAT cell trypsinization. Absorption assays with this supernatant treated with different agents, showed that lipids, simple peptides and nucleic acids were not important components of the antigenic determinants. On the contrary, its susceptibility to beta-galactosidase and particularly to a mild periodate oxidation, suggested that determinants recognized by the IgM against the EAT cell surface are carbohydrate in nature.

Animals↗
PubMed1984

[Stimulation of cell division by Ehrlich carcinoma cell surface antibodies].

Some Ehrlich ascites cancer cells of the mouse show nuclear division as a response to cell surface signals. Antibodies to plasma membrane produce a membrane molecular redistribution, but only 25 per 100 proceed to nuclear division. This division is not associated to DNA synthesis, showing that the effect is produced in G0 phase cells originated from G2 phase cells.

Animals↗
PubMed1982

Disorders of regulatory T cells in patients with selective IgA deficiency and its relationship to associated autoimmune phenomena.

In vitro lymphocyte function of 13 patients with selective IgA deficiency was studied. IgG, IgA and IgM secretion by pokeweed mitogen-stimulated peripheral blood lymphocytes from normal donors and IgA deficient patients was measured by an enzyme-linked immunosorbent assay. Addition of concanavalin A or hydrocortisone and co-cultures of B and T cell enriched populations from patients and normal donors, allowed us to investigate B cell Ig production and T cell regulatory abnormalities. IgA production by these patients' B cells was either absent or very low, as compared to their total Ig production, even in the presence of optimal T cell help. Several T cell immunoregulatory abnormalities were seen in different patients. A moderate increase in suppressor activity selective for IgA production was observed in some, but does not appear to play a major role in the pathogenesis of the IgA deficiency. In others, with associated autoimmune phenomena, a decrease in suppressor T cell function was found.

Adolescent↗
PubMed1982

[Circulating immune complexes in the serum of tumor patients].

The conditions for the detection of circulating immune complexes (CIC) were established by combination of polyethylene glycol precipitation with a nephelometric determination on the precipitate of endogenous C1q. The CIC precipitated from the sera of patients with breast carcinoma, malignant melanoma or autoimmune diseases were dissociated in SDS-beta-mercaptoethanol buffer and no differences were observed in the electrophoretic patterns os polyacrylamide gels allowing to characterize tumour specific antigens.

Antigen-Antibody Complex↗
PubMedDate not supplied

Pseudo-allergic reactions to corticosteroids: diagnosis and alternatives.

Two patients treated with parenteral paramethasone (Triniol) and dexamethasone (Sedionbel) are described. A few minutes after administration of the drugs, they presented urticaria (patients 1 and 2) and conjunctivitis (patient 1). The purpose of our study was to determine the cause of the patients' reactions, the immunological mechanisms involved and whether these patients would be able to tolerate any kind of corticoid. Clinical examinations and skin, oral and parenteral challenges with different corticosteroids and ELISA tests were performed. In the two patients, skin and ELISA tests with paramethasone were negative, as was the prick test with each of its excipients. A single-blind parenteral challenge with Triniol was positive in both patients after the administration of 1 ml of the drug, and negative with its excipients. We also carried out oral and parenteral challenges with other corticosteroids and found intolerance to some of them. These results suggest that paramethasone caused pseudoallergic reactions in our patients. Corticosteroids different from paramethasone also produced hypersensitivity reactions in these patients; however, a few of them were tolerated. The basic mechanisms of those reactions are not yet fully understood. To our knowledge, this is the first report of a pseudo-allergy caused by paramethasone.

Adult↗
PubMedDate not supplied

Severe allergic conjunctivitis and chemosis caused by disodium cromoglycate.

A 63-year-old man with chronic, nonallergic rhinoconjunctivitis presented immediate adverse reactions, such as intense itching, burning, redness and severe swelling of both conjunctivae after using disodium cromoglycate eye drops. Skin prick tests and conjunctival provocation tests were positive with pure disodium cromoglycate. Circulating IgE-specific antibodies to disodium cromoglycate in serum were demonstrated by RAST. We suggest that the acute ocular reaction was caused by disodium cromoglycate and that the underlying mechanism was probably an IgE-mediated immunological reaction.

Conjunctivitis, Allergic↗