cells expressed CD79 and were admixed with considerable amounts of CD3 cells and were considered by the writers to be chronic lymphomatous cells. In our series, the fre-quency of CD20? lymphoid aggregates was 333-345 and showed 65-42 of the H-E good BMBs. In 12 of 1-3 cases, nodules were exclusively or mainly consists of CD3 cells using a stored CD4/CD8 proportion. CD79 cells were plasma cells and sparse Doxorubicin structure activated lymphocytes. Only 1 case presented lots of CD79 cells admixed with CD3 cells in nodules. In this instance, as in the others, BCL2 JH PCR was negative in the BM aspirate received during the time of biopsy, and we regarded these CD79 cells to be hematogones since many of them indicated CD10, TdT, and CD34. Some authors have suggested that the lack of CD20 staining in BMB using immunohistochemistry could result from saturation of the CD20 binding internet sites after the first infusion of rituximab since detectable quantities of free moving rituximab are present for as long as six months after treatment. Besides the fact the BM specimens were obtained long after the last rituximab injection, this hypothesis may be ruled out here for 3 reasons: immunochemistry against human IgG1 was negative, the anti CD20 L26 used in immunochemistry acknowledges a intracytoplasmic epitope not the same as the top epitope bound by rituximab, and molecular Plastid remission, as measured by bone marrow BCL2 JH settlement, had been achieved in every these individuals. There was no correlation between the pres-ence of T cell aggregates and sex, age, initial sample of BM participation, o-r delay between the last rituximab injection and the BM trephines. Curiously, full o-r partial remission was reached for 700-watt of patients with postrituximab T cell nodules versus 52-yard in the 19 patients without BM infiltration. This suggests a specific level of antitumoral immune response in patients having a BM T cell response. This is also in keeping with the observation of macrophages in certain of the patients BMB and also a possible indication of tumor clearance by cytotoxicity. Certainly, antibody mediated antitumoral treatments also stimulate cellular responses against the growth and provide a signal via their cell surface target. Rituximab therapy may also GW0742 promote uptake and cross presentation of lymphoma cell derived peptides by antigen presenting dendritic cells, induce their maturation, and allow the generation of specific antitumor immunity. In summary, T lymphoid nodules morphologically mimicking residual infection aren’t rare in posttherapy BMB specimens from patients with FL treated by rituximab. These infiltrates, which are composed of T cells and from the disappearance of BCL2 JH rearrangement, can be viewed as harmless and possibly as a marker of antitumoral activity. Such images of BM infiltration in control biopsies must therefore always be related to immunochemistry.