FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3022796449> ?p ?o ?g. }

• W3022796449 endingPage "515" @default.
• W3022796449 startingPage "515" @default.
• W3022796449 abstract "Isabelle Douek and colleagues (May 29, p 1850)1Douek IF Leech NJ Gillmor HA Bingley PJ Gale EAM Children with type-1 diabetes and their unaffected siblings have fewer symptoms of asthma.Lancet. 1999; 353: 1850Summary Full Text Full Text PDF PubMed Scopus (76) Google Scholar and the EURODIAB ACE substudy group2EURODIAB ACE Substudy 2 Study GroupDecreased prevalence of atopy in diabetic children.Diabetologia. 1998; 41 (abstr).: A22Google Scholar suggest that low incidence of asthma among patients with type-1 diabetes mellitus is more than coincidental. The T-helper (Th)1/Th2 model suggests that the two diseases are unlikely to co-exist in the same individual because they are dominant immune response is driven by interleukin 2, interferon gamma, and cell-mediated immunity. By contrast, allergic asthma is a Th2 disease in which interleukin 4, interleukin 5, and IgE dominate the immune response. The distinct polarisation of type-1 diabetes and allergic asthma, however, provide a unique opportunity to re-examine the underlying pathogenesis of both diseases and to offer new approaches in the prevention of these diseases.Since the progression of the Th1 or Th2 immune response is closely linked to HLA markers of the host, the susceptible gene for one disease might be a resistant gene for the other disease. Thus, molecular engineering may be possible to alter the susceptibility of individuals who are prone to autoimmune disease such as type 1 diabetes.In an independent metabolic study,3Szczeklik A Pieton R Sieradzki J Alteration in both insulin release and its hypoglycemic effects in atopic bronchial asthma.J Allergy Clin Immunol. 1980; 66: 424-427Summary Full Text PDF PubMed Scopus (13) Google Scholar Szczeklik and colleagues showed that glycaemic responses to tolbutamide or insulin were significantly different between children with atopic asthma and controls. They conclude that more economic use of insulin and reduction in hypoglycaemic effects of cate-cholamines in bronchial asthma might explain why asthmatics rarely develop diabetes. It is tempting to speculate that there is a hidden link between a genetic marker for neurohorminal control and immunological markers that together drive the host to develop either Th1 or Th2 disease.In the Th1/Th2 model, cross-regulation of the Th1 immune response to suppress Th2 disease, or vice versa, is now possible. For instance, bacille Calmette-Guèrin infection can suppress allergic sensitisation.4Herz U Gerhold K Gruber C et al.BCG infection suppresses allergic sensitization and development of increased airway reactivity in an animal model.J Allergy Clin Immunol. 1998; 102: 867-874Summary Full Text Full Text PDF PubMed Scopus (216) Google Scholar Likewise, treatment with interleukin 4 suppresses the onset of type-1 diabetes.5Cameron MJ Arreaza GA Zucker P et al.IL-4 prevents insulitis and insulin-dependent diabetes mellitus in nonobese diabetic mice by potentiating of regulatory T helper-2 cell function.J Immunol. 1997; 159: 4686-4692PubMed Google Scholar The question now is, how long we need to maintain such immunotherapy in patients and what are its long-term consequences?Whatever the answers turn out to be, any immunological intervention has to start early, at the onset or even before the onset of the disease. This early intervention is particularly important for type-1 diabetes, because the effect of therapy will not be felt once the β-cell mass in the diseased pancreas is substantially diminished. Isabelle Douek and colleagues (May 29, p 1850)1Douek IF Leech NJ Gillmor HA Bingley PJ Gale EAM Children with type-1 diabetes and their unaffected siblings have fewer symptoms of asthma.Lancet. 1999; 353: 1850Summary Full Text Full Text PDF PubMed Scopus (76) Google Scholar and the EURODIAB ACE substudy group2EURODIAB ACE Substudy 2 Study GroupDecreased prevalence of atopy in diabetic children.Diabetologia. 1998; 41 (abstr).: A22Google Scholar suggest that low incidence of asthma among patients with type-1 diabetes mellitus is more than coincidental. The T-helper (Th)1/Th2 model suggests that the two diseases are unlikely to co-exist in the same individual because they are dominant immune response is driven by interleukin 2, interferon gamma, and cell-mediated immunity. By contrast, allergic asthma is a Th2 disease in which interleukin 4, interleukin 5, and IgE dominate the immune response. The distinct polarisation of type-1 diabetes and allergic asthma, however, provide a unique opportunity to re-examine the underlying pathogenesis of both diseases and to offer new approaches in the prevention of these diseases. Since the progression of the Th1 or Th2 immune response is closely linked to HLA markers of the host, the susceptible gene for one disease might be a resistant gene for the other disease. Thus, molecular engineering may be possible to alter the susceptibility of individuals who are prone to autoimmune disease such as type 1 diabetes. In an independent metabolic study,3Szczeklik A Pieton R Sieradzki J Alteration in both insulin release and its hypoglycemic effects in atopic bronchial asthma.J Allergy Clin Immunol. 1980; 66: 424-427Summary Full Text PDF PubMed Scopus (13) Google Scholar Szczeklik and colleagues showed that glycaemic responses to tolbutamide or insulin were significantly different between children with atopic asthma and controls. They conclude that more economic use of insulin and reduction in hypoglycaemic effects of cate-cholamines in bronchial asthma might explain why asthmatics rarely develop diabetes. It is tempting to speculate that there is a hidden link between a genetic marker for neurohorminal control and immunological markers that together drive the host to develop either Th1 or Th2 disease. In the Th1/Th2 model, cross-regulation of the Th1 immune response to suppress Th2 disease, or vice versa, is now possible. For instance, bacille Calmette-Guèrin infection can suppress allergic sensitisation.4Herz U Gerhold K Gruber C et al.BCG infection suppresses allergic sensitization and development of increased airway reactivity in an animal model.J Allergy Clin Immunol. 1998; 102: 867-874Summary Full Text Full Text PDF PubMed Scopus (216) Google Scholar Likewise, treatment with interleukin 4 suppresses the onset of type-1 diabetes.5Cameron MJ Arreaza GA Zucker P et al.IL-4 prevents insulitis and insulin-dependent diabetes mellitus in nonobese diabetic mice by potentiating of regulatory T helper-2 cell function.J Immunol. 1997; 159: 4686-4692PubMed Google Scholar The question now is, how long we need to maintain such immunotherapy in patients and what are its long-term consequences? Whatever the answers turn out to be, any immunological intervention has to start early, at the onset or even before the onset of the disease. This early intervention is particularly important for type-1 diabetes, because the effect of therapy will not be felt once the β-cell mass in the diseased pancreas is substantially diminished." @default.
• W3022796449 created "2020-05-13" @default.
• W3022796449 creator A5002424525 @default.
• W3022796449 date "1999-08-01" @default.
• W3022796449 modified "2023-09-29" @default.
• W3022796449 title "Asthma and diabetes" @default.
• W3022796449 cites W1672597967 @default.
• W3022796449 cites W2026220814 @default.
• W3022796449 cites W2063711312 @default.
• W3022796449 cites W2073244493 @default.
• W3022796449 doi "https://doi.org/10.1016/s0140-6736(05)75551-3" @default.
• W3022796449 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10465204" @default.
• W3022796449 hasPublicationYear "1999" @default.
• W3022796449 type Work @default.
• W3022796449 sameAs 3022796449 @default.
• W3022796449 citedByCount "7" @default.
• W3022796449 countsByYear W30227964492012 @default.
• W3022796449 countsByYear W30227964492020 @default.
• W3022796449 crossrefType "journal-article" @default.
• W3022796449 hasAuthorship W3022796449A5002424525 @default.
• W3022796449 hasConcept C126322002 @default.
• W3022796449 hasConcept C134018914 @default.
• W3022796449 hasConcept C177713679 @default.
• W3022796449 hasConcept C2776042228 @default.
• W3022796449 hasConcept C555293320 @default.
• W3022796449 hasConcept C71924100 @default.
• W3022796449 hasConceptScore W3022796449C126322002 @default.
• W3022796449 hasConceptScore W3022796449C134018914 @default.
• W3022796449 hasConceptScore W3022796449C177713679 @default.
• W3022796449 hasConceptScore W3022796449C2776042228 @default.
• W3022796449 hasConceptScore W3022796449C555293320 @default.
• W3022796449 hasConceptScore W3022796449C71924100 @default.
• W3022796449 hasIssue "9177" @default.
• W3022796449 hasLocation W30227964491 @default.
• W3022796449 hasLocation W30227964492 @default.
• W3022796449 hasOpenAccess W3022796449 @default.
• W3022796449 hasPrimaryLocation W30227964491 @default.
• W3022796449 hasRelatedWork W1170641859 @default.
• W3022796449 hasRelatedWork W1563850031 @default.
• W3022796449 hasRelatedWork W2044031531 @default.
• W3022796449 hasRelatedWork W2184851178 @default.
• W3022796449 hasRelatedWork W2415759662 @default.
• W3022796449 hasRelatedWork W2788984504 @default.
• W3022796449 hasRelatedWork W2969988697 @default.
• W3022796449 hasRelatedWork W3036934084 @default.
• W3022796449 hasRelatedWork W4322724676 @default.
• W3022796449 hasRelatedWork W635644365 @default.
• W3022796449 hasVolume "354" @default.
• W3022796449 isParatext "false" @default.
• W3022796449 isRetracted "false" @default.
• W3022796449 magId "3022796449" @default.
• W3022796449 workType "article" @default.