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HERV-K10s and Immune-Mediated (Type 1) Diabetes
Michael S Lan, Andrew Mason, Regis Coutant, Qiao-Yi Chen, Alphonso Vargas, Jayshree Rao, Ricardo Gomez, Stuart Chalew, Robert Garry, Noel K Maclaren Cell Volume 95, Issue 1, Pages (October 1998) DOI: /S (00)
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Figure 1 Detection of HERV-K Viremia in Human Plasma
(A) RT-PCR LTR sequences from patients’ plasma. Plasma RNA preparations from 8 patients with newly onset type 1 diabetes (1–8), 4 with established type 1 diabetes (9–12), and 12 age-matched control patients (13–24) were subjected to RT-PCR with R-poly(A)/U3 primers as described (Conrad et al. 1997). PCR products were separated by electrophoresis and Southern blotted with an LTR cDNA probe. (B) RT-PCR and (C) PCR of total RNA extracted from patient plasma using oligonucleotide primers complementary to IDDMK-22 env sequence. Plasma RNA preparations from the same patients in (A) were subjected to DNase treatment before RT-PCR or PCR reaction. Env sequence primers are 5′-ATGGGTAACACCAGTCACATGG-3′ and 5′-CTAATCTATAATAGTTCCGAATTC-3′. RIC1 cDNA was used as a probe for the hybridization. Signals between patients and controls were similar. Cell , 14-16DOI: ( /S (00) )
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Figure 2 Detection of Antibodies to RIC1 and mouse T cells in a Vβ-specific fashion, as was anticipated from the original data. The precise molecular assignment of Sag function to one or more defined members of the HERV-K family will help to clarify this issue further. It will also facilitate epidemiological studies designed to determine if there is a correlation between the disease at preclinical stages and peripheral Vβ7 expansion and HERV expression. Cell , 14-16DOI: ( /S (00) )
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