Lymphocyte subsets in pre-diabetes.

Abstract

Overwhelming evidence has accumulated in recent years that insulin dependent diabetes mellitus (IDD) is an autoimmune disease occurring in genetically susceptible individuals (1). Evidence for a possible role of humoral immunity in the autoimmunopathogenesis of IDD was initially suggested in the mid-1970’s by the findings of 2 different autoantibodies reactive to either surface (islet cell surface antibodies) or cytoplasmic antigens (islet cell antibodies) (2). The presence of a mononuclear (predominantly lymmphocytic) infiltration of the pancreatic islets had earlier provided evidence for involvement of the cellular arm of the immune system (3). More recently, “activated” T cells have been detected, both in these lymphocytic pancreatic islet infiltrates at the time of diagnosis as well as in recurrent insulitis following pancreatic transplantation (4–5). In addition, multiple defects in T cell mediated immunity (CMI) have been described in one of the prototypic animal model for human IDD, the biobreeding (BE) rat (6). These include severe lymphopenia, abnormal ratio of T lymphocyte subsets, an inability to reject skin grafts across major histocompatibility barriers, reduced proliferative response to T cell mitogens, and the ability to adaptively transfer diabetes.KeywordsBeta CellLymphocyte SubsetIslet Cell AntibodyIslet Cell AutoantibodyFetal IsletThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.