PMID- 16879245 OWN - NLM STAT- MEDLINE DCOM- 20060921 LR - 20181113 IS - 0009-9104 (Print) IS - 1365-2249 (Electronic) IS - 0009-9104 (Linking) VI - 145 IP - 2 DP - 2006 Aug TI - Rotavirus-specific T cell responses and cytokine mRNA expression in children with diabetes-associated autoantibodies and type 1 diabetes. PG - 261-70 AB - Rotavirus infections have been implicated as a possible trigger of type 1 diabetes. We elucidated this connection by comparing peripheral blood T cell responses to rotavirus between children with newly diagnosed type 1 diabetes (n = 43), healthy children with multiple diabetes-associated autoantibodies (n = 36) and control children carrying human leukocyte antigen (HLA)-conferred susceptibility to type 1 diabetes but without autoantibodies (n = 104). Lymphocyte proliferation assays based on stimulation with an antigen were performed using freshly isolated peripheral blood mononuclear cells (PBMC) and IgG and IgA class rotavirus antibodies were measured using plasma samples collected from the children. The expression of interferon (IFN)-gamma, interleukin (IL)-4, IL-10 and transforming growth factor (TGF)-beta in PBMC was studied with real-time polymerase chain reaction (PCR) in a subgroup of 38 children. No differences were observed in the strength or frequency of positive T cell responses to rotavirus between children with overt diabetes, children with multiple autoantibodies and control children. Children with diabetes-associated autoantibodies had, instead, stronger T cell responses to purified coxsackie B4 virus than control children. Rotavirus-stimulated lymphocytes from autoantibody-positive children produced more IL-4 and phytohaemagglutinin (PHA)-stimulated lymphocytes more IL-4 and IFN-gamma than lymphocytes from control children. PHA-stimulated lymphocytes from children with diabetes also produced more IL-4 and purified protein derivative (PPD)-stimulated lymphocytes less TGF-beta than lymphocytes from autoantibody-negative control children. In conclusion, our lymphocyte proliferation studies did not provide evidence supporting an association between rotavirus infections and the development of type 1 diabetes or diabetes-associated autoantibodies in young children. FAU - Makela, M AU - Makela M AD - Immunogenetics Laboratory, University of Turku, Medicity, Biocity 4. krs, Tykistokatu 6A, 20520 Turku, Finland. miia.makela@utu.fi FAU - Oling, V AU - Oling V FAU - Marttila, J AU - Marttila J FAU - Waris, M AU - Waris M FAU - Knip, M AU - Knip M FAU - Simell, O AU - Simell O FAU - Ilonen, J AU - Ilonen J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Clin Exp Immunol JT - Clinical and experimental immunology JID - 0057202 RN - 0 (Antigens, Viral) RN - 0 (Autoantibodies) RN - 0 (Cytokines) RN - 0 (RNA, Messenger) RN - 0 (Transforming Growth Factor beta) RN - 130068-27-8 (Interleukin-10) RN - 207137-56-2 (Interleukin-4) RN - 82115-62-6 (Interferon-gamma) SB - IM MH - Antigens, Viral/immunology MH - Autoantibodies/*immunology MH - Case-Control Studies MH - Cell Proliferation MH - Child MH - Child, Preschool MH - Cytokines/*genetics MH - Diabetes Mellitus, Type 1/*immunology MH - Female MH - Humans MH - Insulin-Secreting Cells/immunology MH - Interferon-gamma/immunology MH - Interleukin-10/immunology MH - Interleukin-4/immunology MH - Linear Models MH - Lymphocyte Activation MH - Male MH - RNA, Messenger/*analysis MH - Reverse Transcriptase Polymerase Chain Reaction MH - Rotavirus/*immunology MH - T-Lymphocytes/*immunology MH - Transforming Growth Factor beta/immunology PMC - PMC1809689 EDAT- 2006/08/02 09:00 MHDA- 2006/09/22 09:00 PMCR- 2007/08/01 CRDT- 2006/08/02 09:00 PHST- 2006/08/02 09:00 [pubmed] PHST- 2006/09/22 09:00 [medline] PHST- 2006/08/02 09:00 [entrez] PHST- 2007/08/01 00:00 [pmc-release] AID - CEI3146 [pii] AID - 10.1111/j.1365-2249.2006.03146.x [doi] PST - ppublish SO - Clin Exp Immunol. 2006 Aug;145(2):261-70. doi: 10.1111/j.1365-2249.2006.03146.x.