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Previous Volume 359:2501-2502 December 4, 2008 Number 23 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: Clatworthy et al. (Aug. 14 issue)¹ report on two patients (one with multiple sclerosis and the other with antineutrophil cytoplasmic antibody–associated vasculitis) in whom anti–glomerular basement membrane nephritis developed after treatment with alemtuzumab. The authors speculate that the emergence of autoreactive B cells rather than persistently suppressed T cells after alemtuzumab therapy might have caused autoimmunity in their patients. However, the production of anti–glomerular basement membrane autoantibodies has been associated with a deficiency of suppressor T cells.² Ligler et al. found that the production of anti–glomerular basement membrane autoantibodies decreased and then stopped as the percentage of . . . [Full Text of this Article]

Related Letters:

Anti–Glomerular Basement Membrane Disease after Alemtuzumab
Clatworthy M. R., Wallin E. F., Jayne D. R.
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N Engl J Med 2008; 359:768-769, Aug 14, 2008. Correspondence

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