摘要：

To investigate the mechanisms triggering MALT-lymphoma development, we examined the occurrence of normal B cells in lymphoid tissue and chronic gastritis with the same idiotype as an IgA-positive MALT lymphoma.Lymphoma idiotype IgA was produced by monoclonal human antibody technology. Against this idiotype a murine monoclonal antibody 27/165 with anti-idiotypic (alpha Id) specificities was raised, and applied immunohistochemically to identify the non-neoplastic precursor B cells in non-neoplastic human tissues.alpha Id 27/165 reacted exclusively with the IgA expressing MALT lymphoma but not with 20 other MALT-type gastric lymphomas nor with 26 nodal lymphomas and was not reactive with normal and inflamed lymph nodes. alpha Id 27/165 immunoreactivity was also absent from MALT of different mucosal sites but was readily encountered on a substantial number of lymphocytes and plasma cells in 95% cases of chronic gastritis associated with Helicobacter pylori (H.p.). The target antigen of the lymphoma IgA was found to be a common antigen of IgA and IgM plasma cells of MALT but not a constituent of bacteria commonly involved in the pathogenesis of gastritis.The distinct binding of alpha Id 27/165 to only reactive mucosal B cells is a first direct evidence for the evolution of MALT-type lymphoma from chronic gastritis. Since the target antigen of the lymphoma IgA has been found to be an autoantigen of MALT plasma cells it is suggested that this MALT-type lymphoma may have arisen after triggering by an autoimmune response resulting from H.p.-induced gastritis.

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