Yazarlar : Audia S, Samson M, Guy J, Janikashvili N, Fraszczak J, Trad M, Ciudad M, Leguy V, Berthier S, Petrella T, Aho-Glélé S, Martin L, Maynadié M, Lorcerie B, Rat P, Cheynel N, Katsanis E, Larmonier N, Bonnotte B.

Yayın : Blood.

Yayın Yılı : 2011

Pubmed Linki : http://www.ncbi.nlm.nih.gov/pubmed/21876120

Konu : Diğer

Literatür İçeriği :  

Abstract

Immune thrombocytopenia (ITP) is an autoimmune disease with a complex pathogenesis. Like in many B cell-related auto-immune diseases, rituximab (RTX) has been shown to increase platelet counts in some ITP patients. From an immunological standpoint, the mode of action of RTX and the reasons underlying its limited efficacy are yet to be elucidated. As splenectomy is a cornerstone treatment of ITP, the immune effect of RTX on this major secondary lymphoid organ were investigated in 18 spleens removed from ITP patients that were treated or not with RTX. Spleens from ITP individuals presented follicular hyperplasia consistent with secondary follicles. RTX therapy resulted in complete B cell depletion in blood and a significant reduction in splenic B cells, whereas these patients did not achieve remission. Moreover, while the percentage of circulating Treg was similar to that in controls, splenic Treg were reduced in ITP patients. Interestingly, the pro-inflammatory Th1 to suppressive Treg ratio was increased in the spleen of patients who failed RTX therapy. These results therefore indicate that although B cells are involved in ITPpathogenesis, RTX induced-total B cell depletion does not correlate with its therapeutic effects, which suggests additional immune-mediated mechanisms of action of this drug.

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