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Patients with AIP are at high risk of having various cancers. The highest risk for cancer in the first year after AIP diagnosis and absence of AIP relapse after successful treatment of the coexisting cancers suggest that AIP may develop as a paraneoplastic syndrome in some patients.

Supplementation with BB536 was well tolerated and reduced UCDAI scores, EI and Mayo subscores after 8 weeks in Japanese patients with mild to moderately active UC.

SUMMARY:We previously reported that autoantibodies against carbonic anhydrase II and lactoferrin are frequently identified in patients with autoimmune-related pancreatitis. To clarify the role of carbonic anhydrase II and lactoferrin, we created animal models of autoimmune pancreatitis by immunizing neonatally thymectomized mice with carbonic anhydrase II and lactoferrin and also by transferring immunized spleen cells to nude mice. Neonatally thymectomized BALB/c mice were immunized with carbonic anhydrase II or lactoferrin followed by three booster injections

The restoration of squamous epithelium after photodynamic therapy (PDT) for Barrett esophagus (BE) and its related neoplasms has been noted. It may result in the development of buried neoplasms and/or BE underneath restored squamous epithelium which maintain their potential for malignant transformation. The purpose of this study was to evaluate the prevalence, endoscopic, and histologic characteristics and also response to further treatment of buried neoplastic epithelium developing after PDT. Fifty-two BE patients with high-grade dysplasia (n=19), intramucosal adenocarcinoma (n=28), and invasive adenocarcinoma (n=5) were treated with porfimer PDT. Buried neoplasms completely covered by squamous epithelium were seen in 1 patient before and in 13 patients after PDT. Their prevalence was 0.6% and 7.4% of pre and post-PDT biopsy levels positive for neoplasia (P=0.001). Buried neoplasms, representing the highest grade of residual neoplasm, were noted in a series of 11 post-PDT endoscopies (7.1% of 155 post-PDT endoscopies with neoplastic diagnoses) of 8 patients. Their occurrence after PDT was neither associated with the length of BE, the diffuseness of neoplasms nor the presence of buried lesions before treatment. There was no prevalent location for these lesions in relation to the original segment of BE, although the majority of both surface and buried neoplasms were found in the prior neoplastic sites. Patients with buried neoplasms responded to further treatment similarly to those with only surface neoplasms (8 of 13 vs. 17 of 24) (P=0.33). In conclusion, buried neoplasms are not uncommon after PDT. Thorough endoscopic surveillance with extensive biopsies, especially of the sites previously positive for neoplasia is important to avoid overlooking buried neoplasms that may progress.

We previously described an animal model of Helicobacter pylori-induced follicular gastritis in neonatally thymectomized (nTx) mice. However, it is still not clear whether antigen-presenting dendritic cells (DCs) in the stomach have a role in the development of secondary follicles in H. pylori-infected nTx mice. We investigated the distribution of DC subsets using this model and examined their roles. To identify lymphoid and myeloid DCs, sections were stained with anti-CD11c (pan-DC marker) in combination with anti-CD8␣ (lymphoid DC marker) or anti-CD11b (myeloid DC marker) and were examined with a confocal microscope. Expression of macrophage inflammatory protein 3␣ (MIP-3␣), which chemoattracts immature DCs, was analyzed by realtime PCR and immunohistochemistry. Follicular dendritic cells (FDCs) were stained with anti-SKY28 antibodies. In noninfected nTx mice, a few myeloid and lymphoid DCs were observed in the bottom portion of the lamina propria, whereas in H. pylori-infected nTx mice, there was an increased influx of myeloid DCs throughout the lamina propria. FDC staining was also observed in the stomachs of members of the infected group. MIP-3␣ gene expression was upregulated in the infected nTx group, and the immunohistochemistry analysis revealed MIP-3␣-positive epithelial cells. These data suggest that H. pylori infection upregulates MIP-3␣ gene expression in gastric epithelial cells and induces an influx of myeloid DCs in the lamina propria of the gastric mucosa in nTx mice. Myeloid DCs and FDCs might contribute to the development of gastric secondary lymphoid follicles in H. pylori-infected nTx mice.Chronic Helicobacter pylori infection induces two distinct types of gastritis, chronic atrophic gastritis and nonatrophic gastritis (4). Nonatrophic gastritis is thought to be a predisposing factor for the development of mucosa-associated lymphoid tissue (MALT) lymphoma (8, 50). The organized structure of the secondary lymphoid tissues is believed to support proper regulation of activation and maturation of the antigen-responsive lymphoid cells (23,24). Although there is a substantial amount of data on the cellular elements that comprise the lymphoid and nonlymphoid components of the secondary lymphatic organs, little is known about the kinetics and roles of dendritic cells (DCs) that establish and maintain the proper organization of the secondary lymphoid tissues.DCs are immune regulatory cells that not only secrete chemokines and cytokines but also present antigens for T cells (39,42,43). In the intestine, DCs are constitutively present in the Peyer's patches, lamina propria, and mesenteric lymph nodes and have an essential role in the uptake of luminar bacterial antigens (37). Because normal gastric mucosa has no mucosaassociated lymphoid system, very little is known about the role of DCs in the mucosal immune system of the stomach, especially their role in H. pylori-induced chronic follicular gastritis.In previous studies (33, 46), it was demonstrated that H. pylori infection of BALB/c mice that were th...

Autoimmune mechanism may be involved in some patients with idiopathic pancreatitis associated with hypergammaglobulinemia.

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