Insulin-dependent diabetes mellitus
Article Abstract:
Insulin-dependent diabetes mellitus (IDDM) has a 50% inheritance factor caused specifically by a class II major histocompatibility complex genotype The antigen-specific type 1 T lymphocyte is considered as a promoting factor for IDDM because it assists in the destruction of Beta cells in the peripheral regions of the kidney. T lymphocytes are also known to produce anti-insulin reactions. The total destruction of Beta cells would then result in a full-blown IDDM. The early detection of beta cell destruction is the best way to prevent the full manifestation of IDDM.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
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Retroviral superantigens and type 1 diabetes mellitus
Article Abstract:
Conrad et al performed a study about the etiological involvement of an infectious agent in type 1 diabetes mellitus. They described the isolation of an unknown endogenous HERV-K10-like retroviral genome, IDDMK(sub 1,2)22, associated with a murine mammary tumor virus whose envelope gene encoded a superantigen. They used the U3-R-poly(A) oligonucleotide primer to detect the retroviral genome. However, in other experiments simulating the experimental conditions employed by Conrad et al, the transcribed genome was not detected and were not RNA specific.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1998
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Development of insulin-dependent diabetes mellitus does not depend on specific expression of the human endogenous retrovirus HERV-K
Article Abstract:
Conrad et al performed a study which cited that the insulin-dependent diabetes mellitus (IDDM) is a beta cell-specific, T cell-mediated autoimmune disease. They suggested that the destruction of the beta cells was through the systemic activation of the autoreactive T cells caused by the expression of superantigen encoded by an endogenous retrovirus, HERV-K. However, there is still no evidence that these superantigens are species specific and in the event that they exist, further examination of their role in IDDM must be conducted.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1998
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