B-Cells in Ocular Adnexal Lymphoproliferative Lesions Express B-cell attracting Chemokine 1 (CXCL13)

Falkenhagen, Katherine M.; Braziel, Rita M.; Fraunfelder, Frederick W.; Smith, Justine R.

doi:10.1016/j.ajo.2005.02.026

Cited by 24 publications

(18 citation statements)

References 7 publications

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“…Importantly, the hypothesis of ocular attraction of Hp-induced gastric lymphoid cells to the inflamed ophthalmic mucosa is also supported by the observation that bilateral ophthalmologic involvement is frequently observed at the diagnosis of OAL (12% in our series) [29] and that a high rate of patients with bilateral and/or more than one MALT site involvement (i.e., 48% of cases) have been reported [9]. In line with this scenario, it is striking to note that blepharitis as also been strongly associated with gastric Hp infection (90% as detected by 13C-urea breath test in a large cohort of patients) [30]. Moreover, it has been reported the expression of the B-cell attracting chemokine 1 (CXCL13) in OAL biopsy specimens [30].…”

Section: Discussionsupporting

confidence: 66%

“…In line with this scenario, it is striking to note that blepharitis as also been strongly associated with gastric Hp infection (90% as detected by 13C-urea breath test in a large cohort of patients) [30]. Moreover, it has been reported the expression of the B-cell attracting chemokine 1 (CXCL13) in OAL biopsy specimens [30]. In the same way, dissociation of first Hp gastric infection and ophthalmologic implantation of activated or lymphomatous cells is in concordance with the lack of efficacy of anti-Hp antibiotic therapy in extragastric MALT localizations [9].…”

Section: Discussionmentioning

confidence: 57%

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Ocular adnexal lymphoma and Helicobacter pylori gastric infection

et al. 2010

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There is a causal association between Helicobacter pylori (Hp) gastric infection and the development of gastric MALT lymphoma. In contrast, the link between Hp gastric infection and the development of extragastric lymphoma has not been thoroughly investigated. We, therefore, studied the prevalence of gastric Hp infection at initial diagnosis of ophthalmologic and nonophthalmologic extragastric lymphoma patients. Three cohorts of patients were studied: a first one of 83 patients with OAL, a second one of 101 patients with extraophthalmologic extragastric lymphoma, and a third one of 156 control individuals (control) without malignant lymphoma. Gastric Hp infection was investigated by histopathological analysis and Hp-specific PCR assay on gastric biopsy tissue samples. We found gastric Hp infection in 37 OAL patients (45%), in 25 extraophthalmologic extragastric lymphoma cases (25%), and in 18 controls individuals (12%) (P < 0.0001 OAL/C and P < 0.01 OAL/extra-OAL cases). Gastritis was found in 51% and 9% of Hp-positive and Hp-negative lymphoma patients, respectively (P < 10 24 ). Gastric Hp infection only correlated with MALT/LPL lymphoma (P 5 0.03). There is a significant association between gastric Hp infection and MALT/LPL OAL. This suggests a novel mechanism of indirect infection-associated lymphomagenesis whereby chronic local antigen stimulation would lead to the emergence of ectopic B-cell lymphoma. Am. J. Hematol. 85:645-649, 2010. V

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 57%

Ocular adnexal lymphoma and Helicobacter pylori gastric infection

et al. 2010

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“…Follicular dendritic cells located in the germinal centers of lymphoid follicles are considered the main source of CXCL13. CXCL13 expression was shown in several B-cell lymphomas, some with extranodal location such as gastric or ocular adnexal lymphomas (3)(4)(5)(6).…”

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confidence: 99%

CXCL13 and CXCL12 in Central Nervous System Lymphoma Patients

Fischer

Korfel

Pfeiffer

et al. 2009

Clinical Cancer Research

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Purpose: Homing of malignant lymphocytes to the central nervous system (CNS) may play a role in the pathogenesis of CNS lymphoma. In this study, we evaluated the chemokines CXCL12 and CXCL13 in the cerebrospinal fluid (CSF) and serum of patients with CNS lymphoma. Experimental Design: Samples from 30 patients with CNS lymphoma (23 with primary and 7 with secondary CNS lymphoma; all B-cell lymphoma) and 40 controls (10 patients with other CNS malignancies and 30 without a malignant CNS disease) were examined. CXCL12 and CXCL13 concentrations were measured using enzyme-linked immunosorbent assays. The grade of blood-brain barrier disruption was estimated by the CSF/serum albumin ratio. Results: CNS lymphoma patients and controls did not differ in CXCL12 serum and CSF levels. Serum levels of CXCL13 were generally low. CXCL13 CSF levels, however, were significantly higher in CNS lymphoma patients as compared with controls (P < 0.0001). Chemokine levels in CSF and serum did not correlate. In CNS lymphoma, CXCL13 concentration in CSF correlated with the degree of blood-brain barrier disruption (R = 0.66; P = 0.003). Elevated CSF levels of CXCL12 and CXCL13 measured in seven CNS lymphoma patients during therapy decreased in five patients who responded to chemotherapy and increased in two with lymphoma progression. Conclusions: Our results suggest a production of CXCL13 within the CNS of CNS lymphoma patients, which decreases with response to therapy. Thus, CXCL13 may represent a marker for further diagnostic and prognostic studies. (Clin Cancer Res 2009;15(19):5968-73)

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“…It would have been of interest to know the incidence of Chlamydia infection or autoimmune disease in the examined OAL cohort; however, it appears that these details were not available to the investigators. To support their hypothesis, however, the authors point out the frequent bilateral involvement of OAL EMZL [25][26][27] and a relatively high incidence of blepharitis in patients with gastric H. pylori [23]. Decaudin et al [24] also propose that, like the autoantigen H(1)K(1)-ATPase, expressed by the gastric epithelium, the lacrimal gland and the gastric may share common epitopes, which could be targets for autoimmune disease.…”

mentioning

confidence: 99%

“…Through this protracted antigenic stimulation, together with interactions with the microenvironment [particularly microorganism-specific T-helper (CD41) and T-regulatory cells] and with the accumulation of genetic alterations resulting in aberrant NF-jB activation, it is suggested that these events ultimately lead to an uncontrolled monoclonal B-cell expansion, which is resistant to inducers of the extrinsic and intrinsic apoptosis pathways [19][20][21]. Recurrent tumor in other extranodal sites is thought to be caused by homing mechanisms involving chemokine receptor and ligand interactions of the lymphoma cells in the required milieu for proliferation [22,23].…”

mentioning

confidence: 99%

A possible new role for Helicobacter pylori in the development of ocular adnexal lymphoma

Coupland

2010

American J Hematol

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B-Cells in Ocular Adnexal Lymphoproliferative Lesions Express B-cell attracting Chemokine 1 (CXCL13)

Cited by 24 publications

References 7 publications

Ocular adnexal lymphoma and Helicobacter pylori gastric infection

Ocular adnexal lymphoma and Helicobacter pylori gastric infection

CXCL13 and CXCL12 in Central Nervous System Lymphoma Patients

A possible new role for Helicobacter pylori in the development of ocular adnexal lymphoma

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