Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to evaluate the polymorphonuclear leukocyte (PMN) function in a poorly controlled adult insulin-dependent diabetic patient (IDDM) with severe recurrent periodontitis, while describing the microbiological and clinical findings. Chemotaxis, superoxide production, and phagocytosis and killing of Porphyromonas (Bacteroides) gingivalis by the IDDM PMN were evaluated 1 week before treatment relative to a healthy, matched control. These analyses revealed a significant (P less than .05) depression in the number of IDDM PMNs migrating along an FMLP gradient (Boyden chamber assay). In addition, a significant (P less than .05) enhancement of IDDM PMN superoxide production in response to opsonized zymosan (cytochrome C reduction) was observed. Phagocytosis and killing (fluorochrome phagocytosis assay) by IDDM PMN of two P. gingivalis strains was also impaired significantly (P less than .05). The subgingival microflora contained significant levels of P. gingivalis, Actinobacillus actinomycetemcomitans, Eikenella corrodens, and Peptostreptococcus micros. Periodontal treatment consisted of extraction of hopeless teeth, scaling and root planing and 3 weeks of Augmentin therapy. The antibiotic therapy resulted in unrecoverable numbers of the putative pathogens and a reduction in both gingival inflammation and disease progression. The IDDM healing response to previous surgical treatment and extractions was poor, presumably due to a marked thrombocytopenia (91 x 10(3) platelets/mm3).
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PMID:Defective neutrophil function in an insulin-dependent diabetes mellitus patients. A case report. 165 89

We have produced a monoclonal antibody 3A4 to the surface of islet cells by fusing spleen lymphocytes from nonobese diabetic (NOD) mice. To identify the molecular weight of specific target antigens reacting with 3A4, 125I-surface-labeled In-111 insulinoma cells were solubilized and extracts were absorbed with 3A4, and immunoprecipitates were followed by polyacrylamide gel electrophoresis and autoradiography. 3A4 recognized two major polypeptides with apparent molecular weights of radioactive 64K and inactive 28K. In order to evaluate the antibody-mediated cytotoxic mechanisms of 3A4, complement-dependent antibody-mediated cytotoxicity (C'-AMC) and antibody-dependent cellular cytotoxicity (ADCC) were tested using a method of specific 51Cr release. In the study for C'-AMC, even over wide ranges of concentration of antibody and rabbit complement, purified 3A4 had no apparent cytotoxic effects on In-111 cells. On the other hand, significant ADCC was observed at an antibody concentration of 10 micrograms/ml and a target:effector cell ratio of 1:40 (P less than 0.01). Finally, the effects of 3A4 on glucose-stimulated insulin release were examined in isolated rat islets. At a glucose concentration of 16.7 mM, 3A4 significantly inhibited the insulin release either in the presence or absence of complement (P less than 0.01). In conclusion, 3A4 could not only bind but also be active to the target cells. Therefore, this monoclonal antibody should be a useful tool to permit a detailed analysis of the pathogenesis of type I diabetes mellitus.
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PMID:Immunochemical characterization of anti-islet cell surface monoclonal antibody from nonobese diabetic mice. 351 30

The production of monoclonal antibodies to islet cell surface antigens, using hybridization of spleen lymphocytes from non-obese diabetic (NOD) mice has been reported previously from our laboratory. In the present study, the immunochemical characteristics of the monoclonal antibody (3A4) have been investigated using In-111 cells, a virus-induced insulinoma cell line derived from the Syrian golden hamster as target cells. The antibody 3A4 could be visually detected in the immunoenzymatic labelling of the surface of In-111 cells. To identify the molecular weight of target specific antigens reacting with 3A4, 125I-surface labelled In-111 cells were solubilized and extracts were absorbed with 3A4. The immunoprecipitates were subjected to polyacrylamide gel electrophoresis and autoradiography. 3A4 recognized two major polypeptides with apparent molecular weights of radioactive 64K and inactive 28K daltons. In order to evaluate antibody-mediated cytotoxic mechanisms of 3A4, complement-dependent antibody-mediated cytotoxicity (C'AMC) and antibody-dependent cellular cytotoxicity (ADCC) were tested, using a method of specific chromium release. In the study for C'AMC, even though over wide ranges of antibody concentration and rabbit complement, purified 3A4 had no apparent cytotoxic effects on In-111 cells. On the other hand, significant ADCC was observed at 10 micrograms/ml antibody concentration and 1:40 target: effector cell ratio. Finally, the effect of 3A4 on glucose-stimulated insulin release in isolated rat islets was examined. At 16.7 mM glucose concentration, 3A4 significantly inhibited the insulin release in the absence or presence of complement. Therefore, 3A4 can not only bind but also be active to the target cells in the cytotoxicity and suppression of insulin release, and it can be a useful tool to clarify the pathogenesis of type 1 diabetes mellitus. Furthermore, these results suggest that the relationship between islet cell surface antibody and cell-mediated immunity, especially immunoresponse against certain antigenic determinants on pancreatic B cells, seems to be important in the pathogenesis of type 1 diabetes mellitus.
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PMID:[Studies on the pathogenesis of type 1 diabetes mellitus--immunochemical studies with monoclonal islet cell surface antibody using hybridization of spleen lymphocytes from non-obese diabetic mice]. 388 86