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At least 577 records · Page 32Linked to original sources
PubMed1982

Study of immunological changes after hyposensitization in house dust sensitive asthmatic children.

The working mechanisms of hyposensitization were studied in 22 asthmatic children who had completed an one-year course of immunotherapy with house dust. Several immunological parameters were followed every four months during the study period. The results showed: (1) There was no significant change in the distribution of total T, active T and B lymphocytes. (2) While the numbers of Tmu and Tgamma cells remained unchanged, their capability to increase after allergen challenge was lost four months after immunotherapy. (3) No change could be found in the total serum IgE, specific IgE and IgG antibodies. Surprisingly enough, the specific IgG antibody, and thus the specific IgG/IgE antibody ratio, decreased in patients who often developed immediate-type asthmatic reactions after allergen shots. (4) The lymphoproliferative response to house dust started to decrease four months after treatment while the mitogenic response to phytohemagglutinin remained the same. (5) The mean percentages of polymorphonuclear leukocytes with Fc and complement receptors were lower than those for normals throughout the study period but the sensitivity of receptor functions to allergen challenge began to decline four months after immunotherapy. Thus this study shows that hyposensitization is able to specifically correct some of the immunological aberrations of the atopic individuals and provides the rationale for the hyposensitization in the treatment of allergic diseases.

Adolescent↗
PubMed1984

Changes of lymphoproliferative responses of T cell subsets to allergen and mitogen after hyposensitization in asthmatic children.

The cellular basis for the mechanism of hyposensitization was studied by examining the changes in the numbers and proliferative responses to house dust and phytohemagglutinin (PHA) of T cell subsets of 25 house dust-sensitive asthmatic children before and 1 yr after hyposensitization. The results demonstrated (1) No difference was observed in the mean percentages of OKT3+ cells and OKT8+ cells between normal subjects and patients both before and after hyposensitization, but the absolute numbers of both types of cells in untreated patients were much higher than in the normal subjects or treated patients because of relative lymphocytosis in the untreated patients, (2) While the mean percentage of OKT4+ cells of the untreated patients was lower than that of the normal subjects (40.8 +/- 4.7% vs 44.8 +/- 4.5%, p less than 0.007), the absolute number was higher in the former than that in the latter because of the same reason. After hyposensitization, the mean percentage of the OKT4+ cells was slightly increased, and (3) Hyposensitization was able to restore the proliferative capability to PHA and depress the sensitivity to specific allergen of OKT4+ cells on the one hand and augment the proliferative responses to both PHA and allergen of OKT8+ cells on the other. Taken together, these immunologic changes may explain partly the suppressed IgE-antibody production and decreased lymphoproliferative response to specific allergen after hyposensitization.

Adolescent↗
PubMed1998

Allergen-specific immunotherapy for allergic rhinitis: a new insight into its clinical efficacy and mechanism.

Immunotherapy has been used widely for allergic diseases for more than 90 years but, in the opinion of many physicians, it is still a controversial form of treatment. The exact mechanism of action of immunotherapy remains to be determined. In the present study, we review the clinical efficacy and mechanism of action of immunotherapy for allergic rhinitis. Recent double-blind placebo-controlled studies have demonstrated the clinical efficacy of immunotherapy for allergic rhinitis. This therapeutic method has several advantages over conventional pharmacological treatment. Immunotherapy is inferior to pharmacological treatment in the short term, but in the long term it is substantially superior with respect to clinical efficacy. Immunotherapy has the potential permanently to alleviate the abnormal immunological responses of allergic rhinitis and to cure the nasal symptoms in the long term, even after discontinuation of injections. In addition, immunotherapy can prevent the onset of new sensitizations in allergic patients and may prevent the progression of rhinitis to asthma. It may therefore be possible for immunotherapy to alter the natural history of allergic sensitization and its clinical manifestation. These lines of clinical evidence could affect strategies of long-term therapy for allergic rhinitis. Modern molecular biological techniques have suggested that immunotherapy may affect allergen-induced TH responses or cytokine profiles, but there is no general agreement among investigators. However, IL-5 is likely to be the most important cytokine involved in the clinical efficacy of immunotherapy, and the suppression of allergen-induced IL-5 synthesis is most likely to be involved in the mechanism of immunotherapy. Our recent investigations, focusing on specific IgE and IgG4 responses, suggest that immunotherapy-induced changes in these specific antibodies play a clinical role and are involved in the mechanism of action of immunotherapy. It is probable that immunotherapy modulates and affects many different immunological and non-immunological phenomena to produce clinical efficacy and that clinical improvement is a consequence of different mechanisms over time.

Allergens↗
PubMed1995

Tryptase and histamine release due to a sting challenge in bee venom allergic patients treated successfully or unsuccessfully with hyposensitization.

BACKGROUND: Hyposensitization with been venom leads to full protection in most, but not all patients with IgE-mediated systemic reactions to bee stings. OBJECTIVE: To determine the relationship of clinical reactivity to the release of mediators and to changes of antibody concentrations in the peripheral circulation at a bee sting challenge test. METHODS: Blood was sampled before (1 min) and at 15, 60 and 180 min after a sting challenge from 19 patients on hyposensitization. Of these six still reacted and 13 were protected. Histamine, mast cell tryptase, bee venom-specific IgE and IgG in the serum, and histamine release from peripheral blood leucocytes (PBL) upon exposure to bee venom were determined. RESULTS: Tryptase above the detection level was found only at 15 (60) min in 4/6 (1/6) patients who reacted. After the sting challenge there was a significant increase of the histamine levels in patients who reacted at 15 min (P < 0.05) and in patients who did react at 60 and 180 min (P < 0.01). The total histamine content of PBL was significantly decreased after 15 and 60 min in patients who reacted (P < 0.01) and in those that did not (P < 0.05). Bee venom-induced histamine release was significantly reduced in patients reacting and those that did not at 15 min (P < 0.05), and was significantly decreased in reactors also at 60 and 180 min (P < 0.05/0.01). Specific IgG antibodies showed a minor decrease (P < 0.05) after the sting challenge in both groups, whereas specific IgE did not change significantly. CONCLUSION: These results indicate that bee venom anaphylaxis is associated with the release of mediators from both mast cells as well as basophils. Successful hyposensitization does not induce a state of immunological non-reactivity, but rather alters the magnitude and the pattern of mediator release.

Adult↗
PubMed1982

Allergic syndrome in chronic cholecystitis and colitis, the efficiency of specific hyposensitivity with microbic allergen.

In more than 1000 patients with noncalculous cholecystitis, chronic colitis (nonulcerative, nonspecific ulcerative, Crohn's disease of the bowel) and with dyskinesia of intestine the participation of allergic components was investigated in the development and chronic duration of the diseases. More often was observed the sensibilization to bacteria of conditionally pathogenetic microflora (E. coli, staphylococcus, streptococcus, proteus) that was confirmed by positive skin tests, sensibilization of lymphocytes to microbic allergens, increase of the titer of microbic antibodies in blood. The sensibilization to tissue proteins and subcellular fractions (nucleus, mitochondrias, microsomes) was seldom observed. Autoimmune disorders appeared in patients with nonspecific ulcerative colitis by ascending doses of bacterial allergens of E. coli, proteus, staphylococcus, streptococcus. By means of the study of direct and remote results of specific immunotherapy there was established the dynamic of clinical and laboratory-instrumental indices of the patients state, and of immunologic tests, reflecting the nonspecific factors of defense, microbic and tissue allergy.

Antigens, Bacterial↗
PubMed2006

[Mechanisms of specific immunotherapy].

Specific immunotherapy (SIT) is a well-established and clinically effective treatment for allergic rhinitis and bronchial asthma. The immunological mechanisms of the subcutaneously applied immunotherapy have been partially elucidated over the past several years but are not completely understood. This report summarizes the immunological and immunoregulatory changes during SIT of wasp venom allergic patients. The induction of IL-10-producing regulatory T cells is described.

Dendritic Cells↗
PubMed1997

Immunotherapy with standardized extract of Dermatophagoides pteronyssinus in bronchial asthma: a dose-titration study.

According to the maximum tolerated dose (MTD) achieved, we assessed the changes in clinical and laboratory parameters, induced by specific immunotherapy (SIT), in a group of 43 asthmatic patients sensitized to Dermatophagoides pteronyssinus, over a period of 18 months. A standardized extract (100 Bu/ml; 40 micrograms/ml of Der p 1; 20 micrograms/ml of Der p 2) was used. The patients were divided into two groups: the high-dose immunotherapy (HDI) group (MTD > or = 4 micrograms Der p I) and the conventional immunotherapy (CI) group (MTD < 4 micrograms Der p 1). Changes in clinical severity index, medication, and symptom scores; in cutaneous and conjunctival reactivity; and in the levels of specific IgE, IgG, IgG1, and IgG4 to D. pteronyssinus (Der p 1 and Der p 2) were measured (ELISA monoclonal antibodies). Safety was monitored according to the EAACI guidelines. The range of the MTD was 0.8-16 micrograms of Der p 1. Ninety percent of the patients tolerated a dose of 3.2 micrograms, but only 18% of the patients reached a maintenance dose of 16 micrograms. The medians of the accumulated dose were 197 micrograms of Der p 1 for the HDI group, and 50 micrograms for the CI group. Conjunctival and cutaneous reactivity was significantly lowered (P < 0.001) after SIT, as were the clinical severity score and medication score in both groups, without significant differences between the groups, except for cutaneous reactivity. Levels of specific IgE decreased significantly (P < 0.01) in both groups, again without significant differences between the groups. The range of the increase in medians of specific IgG, IgG1, and IgG4 was 4.4-120-fold for the HDI group and 3-24-fold for the CI group (P < 0.01). The increase in the levels of Der p 1 and Der p 2 IgG4 were correlated to the changes in cutaneous and conjunctival reactivity (P < 0.01). These results show that a maintenance dose of 3.2 micrograms Der p 1 (8 BU) can induce pronounced clinical and immunologic changes with an excellent safety profile.

Adolescent↗