In this study, we examined lymphocyte homing receptor and vascular addressin expression in a case of primary gastric
B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) with a secondary intestinal spread. We compared the findings with that observed in B cells of normal MALT and MALT acquired as a consequence of Helicobacter pylori-associated
gastritis and other low-grade gastric B-cell
MALT lymphomas. The neoplastic B cells in the gastric
tumor were alpha 4 beta 7-, CD62L+, whereas the intestinal secondary was alpha 4 beta 7+, CD62L-. Incubation of isolated
tumor cells from the stomach by H. pylori generated T-cell-dependent proliferation of neoplastic B cells and induced expression of
alpha 4 beta 7 integrin similar to the intestinal
tumor. These observations indicate that reversal of homing receptor profile in the gastric
tumor by
antigen specific stimulation may be responsible for secondary intestinal dissemination. In normal stomach and normal MALT, alpha 4 beta 7 and CD62L expression reflected the differentiation of the B cell. Plasma cells were alpha 4 beta 7+, CD62L-, whereas a subset of memory B cells were alpha 4 beta 7-, CD62L+. Homing receptor expression in
MALT lymphoma B cells was heterogeneous, however, in line with their memory B-cell phenotype in the majority of cases, the neoplastic B cells were alpha 4 beta 7-, CD62L+. Neoplastic plasma cells were always alpha 4 beta 7+, CD62L-. The venules in normal gastric mucosa expressed mucosal addressin
cell adhesion molecule-1 but not
peripheral lymph node addressin. In normal MALT, H. pylori-associated follicular
gastritis and
MALT lymphomas high endothelial venules coexpressed mucosal addressin
cell adhesion molecule-1 and
peripheral lymph node addressin. These findings suggest expression of
lymphocyte homing receptors by B cells and
vascular addressins by mucosal venules are similar in normal MALT and
MALT lymphomas, and factors controlling normal mucosal B-cell traffic are also operational in
MALT lymphomas.