M. Manghetti

In vivo CD30 expression in human diseases with predominant activation of Th2-like T cells.

CD3O is a member of the tumor necrosis factor (TNF) receptor family, originally described as a marker for Hodgkin and Reed‐Sternberg cells in Hodgkins disease, which has been found to be preferentially expressed by T cells producing Th2‐type cytokines. The presence of CD3O expression was assessed by both immunohistochemistry and reverse transcriptase‐polymerase chain reaction in the target organs of patients with Th1‐ or Th2‐dominated disorders. CD3O expression was found in neither the gut of patients with Crohns disease nor in the gastric antrum of Helicobacter pylori‐infected patients, where there was high interferon‐γ (IFN‐γ) expression. In contrast, high CD3O expression in the apparent absence of IFN‐γ expression was observed in the skin of patients with systemic sclerosis or chronic graft versus host disease (GVHD), which can be considered Th2‐dominated disorders. Moreover, high levels of soluble CD3O were found in the serum of both systemic sclerosis and GVHD patients but not in the serum of patients suffering from multiple sclerosis, a Th1‐dominated disorder. Thus, CD3O expression appears to be preferentially associated with Th2‐type responses not only in vitro but also in vivo. J. Leukoc. Biol. 61: 539–544; 1997.

Impaired T-cell regulation of B-cell growth in Helicobacter pylori–related gastric low-grade MALT lymphoma

BACKGROUND & AIMS Neoplastic B cells of the Helicobacter pylori-related low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma are responsive to T helper cells and sensitive to withdrawal of H. pylori-induced T-cell help. METHODS The clonal progeny of T cells from the gastric mucosa of 5 patients with MALT lymphoma was compared with that of T-cell clones obtained from 5 H. pylori-infected patients with chronic gastritis. RESULTS T-cell clones were assessed for specificity to H. pylori, cytokine profile, help for B-cell proliferation, and perforin- or Fas-mediated cytotoxic regulation of B-cell growth. Twenty-eight of 165 CD4(+) gastric clones from MALT lymphoma and 33 of 178 CD4(+) clones from chronic gastritis recognized H. pylori antigens. Cytokine production was similar in the 2 series of clones. All MALT lymphoma-derived clones dose-dependently increased their B-cell help, whereas clones from chronic gastritis lost helper activity at T-to-B-cell ratios greater than 1 because of concomitant cytolytic killing of B cells. T-cell clones from MALT lymphoma had both reduced perforin-mediated cytotoxicity and poor ability to induce Fas-mediated apoptosis. These defects were limited to gastric T cells. CONCLUSIONS H. pylori-induced T cell-dependent B-cell activation and deficient cytotoxic control of B-cell growth may link H. pylori infection, local T-cell response, and genesis of low-grade gastric MALT lymphoma.

Post-treatment diagnostic accuracy of a new enzyme immunoassay to detect Helicobacter pylori in stools

Helicobacter pylori has attracted increasing attention among gastroenterologists because of its pathogenic potential, stimulating the search for non‐invasive diagnostic tests.