PMID- 9662058 OWN - NLM STAT- MEDLINE DCOM- 19980911 LR - 20190816 IS - 0012-186X (Print) IS - 0012-186X (Linking) VI - 41 IP - 6 DP - 1998 Jun TI - Cellular immune responses to beta casein: elevated in but not specific for individuals with Type I diabetes mellitus. PG - 731-5 AB - Elevated cellular immune responses against the cows' milk protein beta casein have been reported in individuals with Type I diabetes mellitus, a finding supportive of the concept that cows' milk consumption may be causative for the disease. We analysed cellular immune reactivities against beta casein in newly-diagnosed Type I diabetic patients, their immediate autoantibody negative relatives, and unrelated healthy individuals in order to further elucidate the role of anti-beta casein immunity in the pathogenesis of Type I diabetes mellitus. Peripheral blood mononuclear cells were stimulated in vitro with various concentrations of three different beta casein preparations, control antigens (tetanus toxoid, mumps extract) and a mitogen (phytohemagglutinin). The frequency and/or mean simulation index of cellular proliferation against two of the beta casein preparations at high antigen concentrations (i.e. 10 or 50 microg/ml) were significantly higher in newly-diagnosed Type I diabetic subjects compared with autoantibody negative healthy control subjects. However, reactivities against beta casein in the Type I diabetic probands and their autoantibody negative relatives, individuals with a very low-rate of disease development, were almost identical. Cellular immune reactivities to other antigens were similar between the subject groups. In addition to indicating the need for appropriately matched subject populations (e.g. human leukocyte antigen (HLA) matched relatives) when analysing cellular immune responses, these findings support our previous contention that individuals genetically prone to autoimmunity may be deficient in forming tolerance to dietary antigens. However, the significance of anti-beta casein immunity as a specific causative factor in the pathogenesis of Type I diabetes mellitus remains unclear. FAU - Ellis, T M AU - Ellis TM AD - Department of Pathology, University of Florida College of Medicine, Gainesville 32610, USA. FAU - Ottendorfer, E AU - Ottendorfer E FAU - Jodoin, E AU - Jodoin E FAU - Salisbury, P J AU - Salisbury PJ FAU - She, J X AU - She JX FAU - Schatz, D A AU - Schatz DA FAU - Atkinson, M A AU - Atkinson MA LA - eng GR - AI/DK39250/AI/NIAID NIH HHS/United States GR - AI42288/AI/NIAID NIH HHS/United States GR - DK45342/DK/NIDDK NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - Germany TA - Diabetologia JT - Diabetologia JID - 0006777 RN - 0 (Antigens) RN - 0 (Autoantibodies) RN - 0 (Caseins) RN - 0 (HLA Antigens) RN - 0 (Phytohemagglutinins) RN - 0 (Tetanus Toxoid) SB - IM MH - Adolescent MH - Adult MH - Age Factors MH - Analysis of Variance MH - Antibody Formation/*immunology MH - Antigens/immunology/pharmacology MH - Autoantibodies/blood MH - Caseins/administration & dosage/*immunology/pharmacology MH - Cell Division/drug effects/immunology MH - Child MH - Child, Preschool MH - Diabetes Mellitus, Type 1/etiology/genetics/immunology MH - Dose-Response Relationship, Drug MH - Female MH - HLA Antigens/genetics/immunology MH - Humans MH - *Immunity, Cellular MH - Leukocytes, Mononuclear/cytology/drug effects/immunology MH - Male MH - Phytohemagglutinins/immunology/pharmacology MH - Sex Factors MH - Tetanus Toxoid/immunology/pharmacology EDAT- 1998/07/14 00:00 MHDA- 1998/07/14 00:01 CRDT- 1998/07/14 00:00 PHST- 1998/07/14 00:00 [pubmed] PHST- 1998/07/14 00:01 [medline] PHST- 1998/07/14 00:00 [entrez] AID - 10.1007/s001250050976 [doi] PST - ppublish SO - Diabetologia. 1998 Jun;41(6):731-5. doi: 10.1007/s001250050976.