The Microenvironment of Human Peyer’s Patches Inhibits the Increase in CD38 Expression Associated with the Germinal Center Reaction

Guilliano, Mark J.; Foxx‐Orenstein, Amy E.; Lebman, Deborah A.

doi:10.4049/jimmunol.166.4.2179

Cited by 11 publications

(9 citation statements)

References 33 publications

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“…Similar results were obtained with an alternative strategy based on CD138 expression, 18 although this strategy was more difficult to apply to all samples because CD138 was not uniformly expressed on PCs nor was its expression restricted to PCs (data not shown), which is consistent with observations from previous studies on gut samples from HIV-infected patients. 19 Another plasma cell (PC) marker, CD38, also presents difficulties both in the gut 20 and in certain disease settings. 21 Furthermore, the gating strategy was verified by determining the immunoglobulin isotype distribution among the PCs.…”

Section: Resultsmentioning

confidence: 99%

CXCR4/IgG-expressing plasma cells are associated with human gastrointestinal tissue inflammation

Buckner

Moir

Kardava

et al. 2014

Journal of Allergy and Clinical Immunology

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Background We previously reported abnormalities in circulating B cells in patients with chronic granulomatous disease (CGD) and those with HIV infection. Gastrointestinal complications are common to both diseases and likely involve perturbation of immune cells, including plasma cells (PCs). IgA is the most abundant immunoglobulin in the human body, with roles in protection and maintenance of intestinal homeostasis. IgA is produced primarily by PCs residing in mucosal tissues that are also thought to circulate in the blood. Objective We sought to characterize and compare PCs in patients with infectious (HIV) and noninfectious (CGD and Crohn disease) diseases that have been associated with intestinal inflammation. Methods Phenotypic and transcriptional analyses were performed on cells isolated from the blood and colon. Results IgA-secreting CCR10-expressing PCs predominated in the guts of healthy subjects, whereas in patients with HIV, CGD, and Crohn disease, there was a significant increase in the proportion of IgG-secreting PCs. Where intestinal inflammation was present, IgG-secreting PCs expressed reduced levels of CCR10 and increased levels of CXCR4. The intensity of CXCR4 expression correlated with the frequency of IgG-expressing PCs and the frequency of CXCR4+/IgG+ PCs was associated with the severity of intestinal inflammatory disease yet distinct from PCs and plasmablasts circulating in the blood. Conclusions These findings suggest that regardless of the underlying disease, the presence of CXCR4+/IgG+ PCs in the gut is a strong yet localized indicator of intestinal inflammation. Furthermore, our findings suggest that CXCR4+/IgG+ PCs might play a role in immune cell homeostasis during inflammatory processes of the gut.

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Section: Resultsmentioning

confidence: 99%

CXCR4/IgG-expressing plasma cells are associated with human gastrointestinal tissue inflammation

Buckner

Moir

Kardava

et al. 2014

Journal of Allergy and Clinical Immunology

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“…Although tonsillar CD19 ϩ cells represent mainly GC B cells, naive cells are also abundant in the tonsils. 17,18 High expression of KLF4 in naive cells compared with memory B cells has been reported. 9 Thus, we investigated whether low expression of KLF4 in the B lymphomas simply reflects physiologically low levels of KLF4 in their GC progenitors ( Figure 1C).…”

Section: Klf4 Is Epigenetically Silenced In B-cell Lymphomasmentioning

confidence: 99%

KLF4 is a tumor suppressor in B-cell non-Hodgkin lymphoma and in classic Hodgkin lymphoma

Guan

Xie

Leithäuser

et al. 2010

Blood

115

106

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The transcription factor KLF4 may act both as an oncogene and a tumor suppressor in a tissue-depending manner. In T-and pre-B-cell lymphoma, KLF4 was found to act as tumor suppressor. We found the KLF4 promoter methylated in B-cell lymphoma cell lines and in primary cases of B-cell lymphomas, namely, follicular lymphoma, diffuse large B-cell lymphoma, Burkitt lymphoma, and in classic Hodgkin lymphoma (cHL) cases. Promoter hypermethylation was associated with silencing of KLF4 expression. Conditional overexpression of KLF4 in Burkitt lymphoma cell lines moderately retarded proliferation, via cell-cycle arrest in G 0 / G 1 . In the cHL cell lines, KLF4 induced massive cell death that could partially be inhibited with Z-VAD.fmk. A quantitative reverse-transcribed polymerase chain reaction array revealed KLF4 target genes, including the proapoptotic gene BAK1. Using an shRNA-mediated knock-down approach, we found that BAK1 is largely responsible for KLF4-induced apoptosis. In addition, we found that KLF4 negatively regulates CXCL10, CD86, and MSC/ ABF-1 genes. These genes are specifically up-regulated in HRS cells of cHL and known to be involved in establishing the cHL phenotype. We conclude that epigenetic silencing of KLF4 in B-cell lymphomas and particularly in cHL may favor lymphoma survival by loosening cellcycle control and protecting from apoptosis. (Blood. 2010;116(9):1469-1478)

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“…Recent studies have shown only GC B cells of PP in aged mice have normal activation phenotype, i.e. Unlike tonsil, PP GC B cells do not express high levels of CD38, although they could be induced to do so after CD40L, IFNγ and anti B cell receptor (BCR) activation [103]. Tonsilar GC B cells can be isolated on the basis of CD39 or IgD expression [101].…”

Section: Role Of Igm In Mucosal B Cell Memorymentioning

confidence: 99%

“…high CD80 and CD86 and low CD23, CD62L and CD38, and highly mutated IgM genes [100]. Moreover, ligation of β7 can reduce CD38 expression [103]. Moreover, tonsilar centroblasts are CD77hi while centrocytes are CD77lo [102].…”

Section: Role Of Igm In Mucosal B Cell Memorymentioning

confidence: 99%

Generation and Maintenance of Mucosal Memory B Cell Responses?

Vajdy¹

2006

CMC

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The mucosal immune system comprises B cells that can mount potent antibody responses against a variety of mucosal pathogens. Mucosal B cell responses can play a decisive role in protection against mucosal pathogens. Induction of mucosal B cell responses can be achieved through mucosal vaccination. However, mucosal administration of antigens without the use of adjuvants or delivery systems can lead to tolerance rather than immunity, and thus considerable efforts have been focused on development of effective immunopotentiating adjuvants and delivery systems. However, because the ultimate goal of vaccination is the induction and maintenance of immunological memory, the underlying mechanisms for induction of long-term mucosal B cell memory need to be analyzed for the selection of appropriate adjuvants. Moreover, as the antigen unspecific innate immune system invoked by adjuvants contributes significantly to the development of antigen-specific B cell responses, and presumably B cell memory, optimal interaction of B cells with cellular components of the innate immune system is required. To better understand the mechanisms that lead to the induction of mucosal antibody responses, antibodies against single epitopes from specific B cell clones as opposed to antibodies against large poly proteins from multiple B cell clones can be studied. This review deals with the concept of mucosal B cell memory with special emphasis on efforts to devise effective prophylactic or therapeutic vaccines.

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The Microenvironment of Human Peyer’s Patches Inhibits the Increase in CD38 Expression Associated with the Germinal Center Reaction

Cited by 11 publications

References 33 publications

CXCR4/IgG-expressing plasma cells are associated with human gastrointestinal tissue inflammation

CXCR4/IgG-expressing plasma cells are associated with human gastrointestinal tissue inflammation

KLF4 is a tumor suppressor in B-cell non-Hodgkin lymphoma and in classic Hodgkin lymphoma

Generation and Maintenance of Mucosal Memory B Cell Responses?

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