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Results for “Desensitization, Immunologic”

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At least 109 records · Page 6Linked to original sources
PubMed1985

Aspirin-sensitive asthma: abnormal platelet response to drugs inducing asthmatic attacks. Diagnostic and physiopathological implications.

The pathogenesis of aspirin-sensitive asthma remains unknown. Using a new model of platelet activation, initially described as a response of platelets to IgE antibody-dependent stimuli, this study was designed to test the hypothesis of a possible involvement of platelets in aspirin-sensitive asthma. Washed platelets from 35 aspirin-sensitive asthmatics showed an abnormal in vitro response to cyclooxygenase inhibiting nonsteroidal anti-inflammatory drugs (NSAIDs)--aspirin, indomethacin or flurbiprofen--characterized by the generation of a cytocidal supernatant and (14 patients explored) a burst of chemiluminescence; these drugs had no similar effect on platelets from 31 controls (p less than 0.0001). It was shown that the abnormal platelet response to NSAIDs was not mediated by IgE. In contrast to platelets, aspirin-sensitive asthmatic leukocytes generated neither cytocidal factors nor chemiluminescence in the presence of NSAIDs. Sodium salicylate and salicylamide, which, though structurally similar to aspirin, do not inhibit cyclooxygenase and are well tolerated by aspirin-sensitive asthmatics, did not activate their platelets to release cytocidal factors. Moreover, preincubation of platelets with sodium salicylate, salicylamide or prostaglandin endoperoxide PGH2, highly prevented their abnormal response to NSAIDs (greater than 80%; p less than 0.0001). Since several lipoxygenase inhibitors (NDGA, esculetin), including inhibitors of both cyclooxygenase and lipoxygenase (ETYA, BW755c), did not activate patient platelets and prevented the subsequent abnormal response to NSAIDs, it is suggested that the abnormal platelet activation by NSAIDs is not only the consequence of an inhibition of cyclooxygenase, but also involves generation of lipoxygenase metabolites of arachidonate. Besides, platelets from 4 aspirin-sensitive asthmatics undergoing aspirin desensitization were found to have completely lost their abnormal responsiveness to NSAIDs. These findings represent the first identification in aspirin-intolerant asthmatics of a specific abnormal cellular response to drugs inducing asthmatic attacks and open new perspectives into the pathogenesis, prevention and diagnosis of this disease. They also provide support to the concept of a role for platelets in asthma.

Adult↗
PubMed1983

The role of cyclic AMP in modulating cytotoxic T lymphocytes. II. Sequential changes during culture in responsiveness of cytotoxic lymphocytes to cyclic AMP-active agents.

Agents that increase cyclic AMP (cAMP) levels inhibited the activity of cytotoxic T lymphocytes (CTL) obtained from spleens of mice immunized with allogeneic cells. Cultured CTL, however, were desensitized to cAMP-active agents, in that the capacity of these agents to inhibit the activity of cultured CTL was markedly reduced. The capacity to inhibit CTL activity was reduced more rapidly for some agents than for others; the percent inhibition by histamine and PGE2 was reduced after 4 hr and was reduced more than 20% after 24 hr, whereas the percent inhibition by dibutyryl cAMP, theophylline, and cholera enterotoxin was reduced less than 6% after 24 hr, and was reduced significantly only after 48 hr. Culture in the presence of antigen accelerated desensitization to the latter three agents. CTL populations were also tested for their capacity to increase cAMP levels in response to agonists. The capacity of histamine to increase cAMP levels of the CTL was lost within 4 hr (i.e., as rapidly as its capacity to inhibit CTL activity) and was never restored, whereas the capacity of PGE2 to increase cAMP levels persisted throughout culture. These results suggest that culture induces multiple alterations in cAMP metabolism of CTL. These alterations, which result in dissociation of CTL activity from cAMP-mediated regulatory steps, may include loss of histamine receptors and/or histamine receptor-adenylate cyclase coupling, and also loss of one or more biochemical reactions that link elevated cAMP levels to inhibition of lysis.

Animals↗
PubMed1971

In vitro desensitization of sensitized murine lymphocytes by a serum factor (soluble antigen?).

The possibility that lymphocytes sensitized to cell-associated antigens may be rendered hyporeactive toward cells expressing these antigens by prior incubation with such antigens in soluble form was investigated. Mice were sensitized to the foreign histocompatibility antigens of an allogeneic strain of mice; lymphocytes from such sensitized mice were incubated with serum from normal mice of the sensitizing, sensitized, and F(1) hybrids of the two strains. These lymphocytes were washed and their in vitro activity against preparations of cells of sensitizing strain origin was measured by modifications of a standard assay. Sera from the sensitizing strain, and from F(1) hybrids of the sensitizing and sensitized strains (which would be expected to contain the soluble histocompatibility antigens to which the lymphocytes were sensitized), abrogated the in vitro activity of lymphocytes against target cells of the sensitizing strain, while serum from the sensitized strain did not. Soluble tumor-specific or histocompatibility antigens may be responsible in part for the specific abrogation of sensitized lymphocyte activity by serum from tumorbearing, successfully allografted, allogeneically pregnant, or chimeric animals.

Animals↗
PubMed2005

Post-transplant therapy with high-dose intravenous gammaglobulin: Applications to treatment of antibody-mediated rejection.

B-cells and their products (antibodies) are now recognized as important mediators of allograft rejection. This represents a significant departure from previous doctrine where the T-cells were felt to be of paramount importance. Antibody-mediated rejection (AMR) has emerged as a significant and common complication of transplantation. The development of donor-specific (anti-HLA class I and class II) antibodies is known to correlate strongly with the development of AMR. Recognition of the unique features of AMR that were often confused with non-specific acute tubular injury is aided considerably by improvements in monitoring of anti-HLA antibodies and the immunopathologic demonstration of C4d staining in affected capillary beds. Although imperfect, the demonstration of C4d (a complement breakdown product) staining in an allograft, especially accompanied by the presence of anti-HLA antibodies in the recipient sera, strongly suggests a diagnosis of AMR. Thus, AMR is a complement-dependent, antibody-mediated disorder. AMR can occur as a de novo complication of transplantation in individuals not previously recognized to be sensitized to HLA antigens, but more often occurs as a complication of desensitization therapies in highly-HLA sensitized patients. AMR may also constitute a significant portion of what is now referred to as chronic allograft nephropathy (CAN). The prognosis of C4d (+) AMR is poor as current therapies for treatment of AR are directed primarily at the T-cell. Until recently, no therapeutic options existed to address this problem from a primary etiological standpoint. Here we discuss the use of high dose IVIG as an option for treatment of AMR. We have significant experience with this approach which is outlined here. IVIG has many ideal advantages as a therapy for AMR. First, it can down regulate B-cell activation and antibody production, second, it can induce anti-inflammatory cytokines and contains blocking antiidiotyic antibodies to anti-HLA antibodies and third, IVIG has the unique ability to block complement-mediated injury through inhibition of C3 activation. Further clinical trials are necessary to prove efficacy for treatment of AMR.

Antibody Specificity↗
PubMed2006

State of the art in developing allergen vaccines in Cuba: prospects of novel adjuvanted vaccines.

Standardized allergen vaccines have been developed and registered as biopharmaceutical products in Cuba. Three different vaccines were obtained from the most relevant allergenic mite species: Dermatophagoides pteronvssinus, Dermatophagoides siboney, and Blomia tropicalis. Immuno-analytical methods based on murine monoclonal antibodies and human IgE antibodies were developed for assessing allergenic potency, composition, and stability. Preclinical and clinical studies showed efficacy and safety in diagnostic prick-tests and subcutaneous immunotherapy in asthmatic patients. New approaches are now undertaken in order to develop new adjuvanted formulations based on liposomes or proteoliposomes from Neisseria meningitidis, and purified allergens; aiming to overcome the drawbacks of conventional immunotherapy.

Adjuvants, Immunologic↗
PubMed1984

A comparison of the clinical and immunological effects of an alum-precipitated five-grass extract with a conjugated two-grass extract in the desensitization of hay fever.

Thirty-nine patients with pollen hay fever were randomly allocated to receive either an alum-precipitated five-grass extract (Allpyral) or a two-grass conjugated extract (Conjuvac) prior to the 1982 pollen season. Efficacy was assessed by means of symptom scores, drug usage and specific IgE and IgG antibody response. Both nasal and eye symptom scores were significantly higher during the pollen season in those patients receiving Allpyral. Specific IgE and IgG measured after the pollen season showed similar rises in each group. Seven patients showed a marked elevation in specific IgE and nine a marked elevation in specific IgG, but no patient showed both. Those with a high specific IgE level tended to be younger. Symptom scores bore no relation to either specific IgE or IgG antibodies. Side-effects were mainly local and were equal in both groups.

Adolescent↗
PubMed1992

Oral administration of immunomodulators and the mucosal immune system.

Orally administered antigens reach the lymphoid tissue in Peyer's patches in the gut where they initiate an immune response with clonal expansion of antigen-specific T and B cells. Activated T cells migrate through lymph and blood to intestinal epithelium (intra-epithelial leukocytes) whereas activated B cells migrate to the lamina propria, other mucosae and exocrine glands where they differentiate into plasma cells secreting polymeric IgA1 or IgA2. These antibodies are transported across the epithelial cells after binding to a poly-Ig receptor, then excreted in the lumen as secretory IgA. Reciprocal interactions have been demonstrated between lymphoid and epithelial cells in the mucosae. Oral administration of antigens in different experimental models may induce the production of secretory antibodies and/or systemic unresponsiveness with suppression of delayed-type hypersensitivity or specific IgG and IgE antibody production or both. New strategies are currently being explored for the development of oral vaccines using recombinant antigens or viral vectors (e.g. pox-viruses, vaccinia virus, cholera toxin B subunit etc.). Conversely, immunomodulating compounds or procedures which could enhance specific oral tolerance in association with antigen would have considerable therapeutic applications in auto-immune diseases and allergy.

Adjuvants, Immunologic↗
PubMed1986

Immunological control of immunotherapy in asthma.

Immunotherapy of allergic diseases first called desensitization or hyposensitization is based on the introduction by parenteral administration or perhaps also by mouth of the allergens which has been considered to be responsible by the clinical symptoms. Immunotherapy partially corrects the imbalance of immune response decreasing IgE response and increasing the production of IgG1 and IgG4 antibodies either by direct effect or by an effect on specific T helpers and T suppressors subsets.

Asthma↗