Allogenic bone marrow transplantation: not a treatment yet for familial Mediterranean fever.

induced immunosuppression is much more likely to be via suppression of humoral immunity, which may take many months to normalize after exposure.4 In pointing out our error, it does highlight the importance of the interplay between these 2 arms of the immune system, and also the effect of combining therapies that may influence both Band T-cell immunity. Indeed, there are recent worrying reports of infections occurring after rituximab administration that are more typically associated with T-cell immunosuppression. Most striking are those of JC papovavirus–related progressive multifocal leukoencephalopathy and cytomegalovirus infection in patients who received periautotransplantation rituximab. Moreover, these patients had an unusually prolonged depression of CD4 cell counts.5 Delayed CD4 cell reconstitution has been reported by others in patients receiving rituximab after autologous transplantation.6 Although there may be other reasons contributing to alterations in T-cell immunity in these reports, they highlight that one should not currently dismiss rituximab’s potential influence, either quantitatively or qualitatively, on T-cell immunity. Unfortunately, many of the described cases of opportunistic infections in patients treated with rituximab do not report T-cell subsets. Indeed, with the increasing use of rituximab, particularly in combination with therapies that are known to alter T-cell immunity, physicians should carefully consider rituximab’s potential immunosuppressive effects. Furthermore, in an attempt to clarify the impact of rituximab on T-cell immunity, further studies quantitating T cells are warranted.