Abstract
Monocytoid B cells are IgM(+) , IgD(-/+) , CD27(-) B cells, localized in the perisinusoidal area of the lymph node. These cells are especially prominent in infections such as those caused by toxoplasma and HIV. The ontogeny of monocytoid B cells with respect to B cell maturation is incompletely known. We analysed clonal expansion, somatic hypermutation and expression of activation-induced cytidine deaminase (AID) in monocytoid B cells. Sequence analysis of the rearranged immunoglobulin heavy chain genes amplified from microdissected monocytoid B cell zones with a high proportion of proliferating cells reveals the presence of multiple clones with low-level ongoing mutations (mean frequency: 0.46 × 10(-2) per bp). Mutation analysis of these ongoing mutations reveals strand bias, a preference of transitions over transversions as well as the occurrence of small deletions, as observed for somatically mutated immunoglobulin genes in the human germinal centre. Proliferation, ongoing mutation as well as expression of AID, combined, is evidence that monocytoid B cells acquire the mutations in the extrafollicular perisinusoidal area of the lymph node and pleads against a postgerminal centre B cell origin.
Highlights
1.3.2 B-cell lymphomas and cell of origin1.3.3 Oncogene translocations in B-cell lymphomas1.3.4 Infection and lymphomagenesis1.3.5 BCR signaling and lymphomagenesis1.4 Marginal zone lymphoma1.4.1 MALT lymphoma1.4.2 Gastric MALT lymphoma and Helicobacter pylori: a model for chronic infection-driven B-cell lymphomagenesis1.4.3 Ocular adnexal lymphoma and Chlamydia psittaci1.4.4 Immunoproliferative small intestinal disease and Campylobacter jejuni1.4.5 Primary cutaneous B-cell lymphoma and Borrelia burgdorferi1.4.6 MALT lymphoma and Autoimmunity
In this study we have examined the mutation status of genes involved in the NF-NB signaling pathway
Although Splenic marginal zone lymphoma (SMZL) shows few mutations of NF-NB signaling genes, our results indicate that the presence of these mutations is associated with a higher histological grade
Summary
1.3.2 B-cell lymphomas and cell of origin1.3.3 Oncogene translocations in B-cell lymphomas1.3.4 Infection and lymphomagenesis1.3.5 BCR signaling and lymphomagenesis1.4 Marginal zone lymphoma1.4.1 MALT lymphoma1.4.2 Gastric MALT lymphoma and Helicobacter pylori: a model for chronic infection-driven B-cell lymphomagenesis1.4.3 Ocular adnexal lymphoma and Chlamydia psittaci1.4.4 Immunoproliferative small intestinal disease and Campylobacter jejuni1.4.5 Primary cutaneous B-cell lymphoma and Borrelia burgdorferi1.4.6 MALT lymphoma and Autoimmunity. 1.4.2 Gastric MALT lymphoma and Helicobacter pylori: a model for chronic infection-driven B-cell lymphomagenesis. Marginal zone lymphoma (MZL) is a non-Hodgkin lymphoma that likely develops from Blymphocytes in the marginal zone of secondary lymphoid tissue. There are three subtypes of marginal zone B-cell lymphoma (MZL) : nodal, extra-nodal and splenic marginal zone lymphoma, arising in the lymph node, mucosa and the spleen, respectively. Splenic marginal zone lymphoma (SMZL) is an indolent, low grade B-cell lymphoma primarily characterized by splenomegaly with variable involvement of lymph nodes, bone marrow, peripheral blood and other organs. It accounts for less than 1% of non-Hodgkin lymphoma. In parallel, unmutated as well as mutated immunoglobulin heavy chain genes are found
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