B-1 cells contribute to plasma cell accumulation in Lyn-/- mice

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Presentation Time: 02:15 PM - 03:30 PM
Poster Board Number: B608
Abstract ID: 5877

Presenting Author:
Anne Satterthwaite , Associate Professor at Univ. of Texas Southwestern Med. Ctr.

Abstract:

The autoimmune disease systemic lupus erythematous is characterized by the production of pathogenic autoantibodies that drive inflammation and tissue damage.  Defining which B cell subsets give rise to these autoantibodies may reveal therapeutic strategies that target pathogenic B cells while sparing responses to immunization and infection.  Mice lacking the tyrosine kinase Lyn develop lupus-like autoimmune disease and accumulate autoreactive plasma cells in the spleen.  We hypothesized that preventing plasma cell formation in Lyn-/- mice would result in an accumulation of cells that would have otherwise terminally differentiated.  Deleting IRF4, a transcription factor required for plasma cell differentiation, from Lyn-/- mice resulted in a dramatic increase in B-1 cells in the peritoneal cavity and the spleen.  B-1 cells are an innate-like subset of B cells that produces natural antibody and has been suggested to play both protective and pathogenic roles in autoimmune and inflammatory disease.  A B-1 cell cre-reporter labeled about half of the splenic plasma cells in Lyn-/- mice, suggesting that B-1 cells may contribute to autoantibody production in this lupus model.   Ongoing studies are aimed at determining the degree of autoreactivity of these labeled plasma cells in comparison to that of the B-1 cells that accumulate in Lyn-/-IRF4-/- mice.