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Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS) caused by complex gene-environment interactions.  ATXN1  maps to 6p22.3, within the 233 loci associated with an increased risk of developing MS. Toxic gain-of-function mutations in  ATXN1  cause the neurodegenerative disorder spinocerebellar ataxia type 1 (SCA1). Conversely,  ATXN1  loss-of-function is involved in Alzheimer’s disease (AD) and tumorigenesis. We have recently shown that  ATXN1  exerts a protective immunomodulatory activity in the MS model experimental autoimmune encephalomyelitis (EAE). Specifically, we demonstrated that mice lacking  Atxn1  experience aggravated EAE due to aberrant B cell functions.  Atxn1 -null mice exhibit increased B cell proliferation with the concomitant expansion of specific B cell subsets including B-1a cells. This population of B cells is responsible for the production of natural immunoglobulins and has been associated with the etiology of multiple autoimmune diseases. To understand the role played by  Atxn1  in these cells, we performed comprehensive transcriptomic profiling of  Atxn1 -null B-1a cells before and after stimulation with an encephalitogenic antigen. Importantly, we show that in this sub-population  Atxn1  regulates immunoglobulin gene transcription and signaling through the B cell receptor (BCR).

The novel multiple sclerosis susceptibility gene ATXN1 regulates B cell receptor signaling in B-1a cells