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Presents a study which shows that high levels of wild-type ataxin-1 can cause degenerative phenotypes similar to those caused by the expanded protein. Genetic screens which were conducted to identify genes that modify spinocerebellar ataxia type 1-induced neurodegeneration; Findings, which may be relevant to the treatment of polyglutamine diseases and, perhaps, to other neurodegenerative diseases.

Discusses research which examined the subcellular localization of wild-type human ataxin-1 and mutant ataxin-1 in the Purkinje cells of transgenic mice. Definition of spinocerebellar ataxia type 1 (SCA1); Results; Normal and mutant ataxin-1 localization compared; COS-1 cells transfected with mutant ataxin-1; Results of colocalization studies; Nuclear matrix preparations; SCA1 pathogenesis. INSET: Methods..

Human and simian immunodeficiency viruses (HIV and SIV) exploit follicular lymphoid regions by establishing high levels of viral replication and dysregulating humoral immunity. Follicular regulatory T cells (TFR) are a recently characterized subset of lymphocytes that influence the germinal centre response through interactions with follicular helper T cells (TFH). Here, utilizing both human and rhesus macaque models, we show the impact of HIV and SIV infection on TFR number and function. We find that TFR proportionately and numerically expand during infection through mechanisms involving viral entry and replication, TGF-β signalling, low apoptosis rates and the presence of regulatory dendritic cells. Further, TFR exhibit elevated regulatory phenotypes and impair TFH functions during HIV infection. Thus, TFR contribute to inefficient germinal centre responses and inhibit HIV and SIV clearance. [ABSTRACT FROM AUTHOR]