Laura Tran in The Scientist:
In the 13th century, unusual skin lesions resembling wolf bites led to the term “lupus,” meaning “wolf” in Latin. These symptoms also took the form of a butterfly across the face and to other parts of the body, hinting at a deeper, more complex condition. Centuries later, researchers provided evidence of lupus as an autoimmune disease, in which overactive T and B cells turn against one’s own body.
Upon activation, B cells undergo differentiation through the germinal center (GC) or extrafollicular (EF) pathways. Notably, those from the EF pathway are a prominent source of autoantibody production, but the mechanism behind their development from naive cells into this state is not fully understood.1 This motivated immunologist Michael Carroll at Harvard Medical School to pinpoint key factors that drive this process.
More here.
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