Anti-CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter infection

Yamamoto, Kōji; Nishiumi, Shin; Yang, Lin; Klimatcheva, Ekaterina; Pandina, Tracy; Takahashi, Shinichi; Matsui, Hidenori; Nakamura, Masahiko; Zauderer, Maurice; Yoshida, Masaru; Azuma, Takeshi

doi:10.1038/mi.2014.14

Cited by 44 publications

(41 citation statements)

References 58 publications

(71 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The involvement of the chemokine CXCL‐13 in gastric MALT lymphoma development in H. suis ‐infected mice was confirmed by administration of an anti‐CXCL‐13 antibody, which was able to reduce the formation of lymphoid follicles and germinal centers . Similar results were obtained by administering VEGF receptor antibodies to infected mice .…”

Section: Experimental Infection With Non‐h Pylori Helicobacterssupporting

confidence: 52%

Gastric and Enterohepatic Helicobacters other than Helicobacter pylori

et al. 2014

View full text Add to dashboard Cite

During the past year, research on non-Helicobacter pylori species has intensified. H. valdiviensis was isolated from wild birds, and putative novel species have been isolated from Bengal tigers and Australian marsupials. Various genomes have been sequenced: H. bilis, H. canis, H. macacae, H. fennelliae, H. cetorum, and H. suis. Several studies highlighted the virulence of non-H. pylori species including H. cinaedi in humans and hyperlipidemic mice or H. macacae in geriatric rhesus monkeys with intestinal adenocarcinoma. Not surprisingly, increased attention has been paid to the position of Helicobacter species in the microbiota of children and animal species (mice, chickens, penguins, and migrating birds). A large number of experimental studies have been performed in animal models of Helicobacter induced typhlocolitis, showing that the gastrointestinal microbial community is involved in modulation of host pathways leading to chronic inflammation. Animal models of H. suis, H. heilmannii, and H. felis infection have been used to study the development of severe inflammation-related pathologies, including gastric MALT lymphoma and adenocarcinoma.

show abstract

Section: Experimental Infection With Non‐h Pylori Helicobacterssupporting

confidence: 52%

Gastric and Enterohepatic Helicobacters other than Helicobacter pylori

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Experimental evidence supporting a role for the lymphoid chemokines in driving “lymphoid neogenesis” comes in part from studies using transgenic mice where overexpression of CCL21 or CXCL13 in organs such as the pancreas or thyroid gland is sufficient to generate ectopic lymphoid structures and cause diabetes or thyroiditis, respectively [16–19]. CXCL13 is found in naturally occurring gastric mucosa-associated lymphoid structures that develop in response to chronic Helicobacter pylori infection [20], and CXCL13-CXCR5 interactions contribute to the development of both H. pylori -associated gastritis and gastric lymphomas [20–23]. Thus, ectopic lymphoid follicles that form via local expression of CXCL13 could be a natural feature of chronic organ-specific inflammation [15,24–27].…”

Section: Cxcl13 Participates In Non-lymphoid Tissue Inflammationmentioning

confidence: 99%

Regulated Production of CXCL13 within the Central Nervous System

Irani¹

2016

J Clin Cell Immunol

View full text Add to dashboard Cite

The chemokine, C-X-C motif ligand 13 (CXCL13), is constitutively expressed in lymphoid organs and controls the recruitment and compartmentalization of lymphocytes and antigen presenting cells within these specialized structures. Recent data, however, also show induction of this molecule under a variety of circumstances during central nervous system (CNS) inflammation. While its role(s) in the pathogenesis of neoplastic, infectious and autoimmune disorders of the CNS remain incompletely understood, growing evidence suggests that CXCL13 could become a relevant therapeutic target in at least some of these conditions. This review focuses on the diseases, cellular sources and external factors known to regulate CXCL13 production in the inflamed CNS.

show abstract

“…CXCL13 has been specifically associated with TLS development. Ectopic CXCL13 expression is sufficient for recruiting B cells and inducing TLS formation in nonlymphoid tissues (13), while inhibiting CXCL13 disrupts their formation (14). In murine secondary lymphoid organs, CXCL13 is principally produced by stromal cells resident in B cell follicles, including follicular DCs (FDC) (15) and marginal reticular cells (the latter absent in TLS) (16).…”

Section: Cd3 + Cd4mentioning

confidence: 99%