Viral Interleukin 6 Stimulates Human Peripheral Blood B Cells That Are Unresponsive to Human Interleukin 6

Breen, Elizabeth C.; Gage, Julia R.; Guo, Beichu; Narazaki, Masashi; Kishimoto, Tadamitsu; Miles, Samuel I.; Martı́nez-Maza, Otoniel

doi:10.1006/cimm.2001.1852

Cited by 19 publications

(9 citation statements)

References 38 publications

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“…Cellular responsiveness to human interleukin 6 (hIL6) requires the expression of two receptor molecules: IL6-specific receptor and a nonspecific signal-transducing molecule. Regulation of responsiveness to hIL6 is generally controlled by IL6-specific receptor expression (Breen et al, 2001). Seven novel single nucleotide polymorphisms (SNPs) were identified (Fig.…”

Section: Resultsmentioning

confidence: 99%

Identification of novel SNPs in the interleukin 6 receptor gene (IL6R)

et al. 2003

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The human interleukin-6 receptor (IL6R) is responsible for signal transduction of IL6 that might have associations with immune diseases and various infectious diseases. We have sequenced all 10 exons including the putative splicing site to identify single nucleotide polymorphisms in IL6R. Seven novel single nucleotide polymorphisms (SNPs) were identified; one SNP in the promoter region (-183G>A), one synonymous SNP in exon 2 (24013G>A: Ala31Ala), one non-synonymous SNP in exon 9 (48892A>C: Asp358Ala) and four in introns (29753A>C, 42700T>C, 48869T>A and 59818C>T). The frequencies of each SNP in the Korean population (n=300) were 0.48 (-183 G>A), 0.13 (24013 G>A), 0.41 (29753A>C), 0.41 (42700T>C), 0.1 (48869T>A), 0.42 (48892A>C), and 0.07 (59818C>T), respectively. Haplotypes and their frequencies were estimated by the EM algorithm. Linkage disequilibrium coefficients (/D'/) between each SNP pair were also calculated. The information on SNPs and haplotypes in IL6R would be useful for genetic studies of this gene.

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Section: Resultsmentioning

confidence: 99%

Identification of novel SNPs in the interleukin 6 receptor gene (IL6R)

et al. 2003

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“…4A). This lower CD126 expression suggests that IL-6 stimulation could be distinct in these populations (55).…”

Section: ϫ Igg ϩ Cells Are Present In Human Bloodmentioning

confidence: 95%

A New Memory CD27−IgG+ B Cell Population in Peripheral Blood Expressing VH Genes with Low Frequency of Somatic Mutation

Fecteau

Côté

Néron

2006

The Journal of Immunology

269

254

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In humans, up to 40% of peripheral B cells express CD27 and have hypermutated variable regions in their Ig genes. The CD27+ B cells are considered to be derived from germinal center following specific antigenic stimulation. Actually, somatic hypermutation in Ig genes and CD27 expression are hallmarks of memory B cells. However, the blood IgM+IgD+CD27+ B cells were recently associated to splenic marginal zone B cells and proposed to be a subset distinct from germinal center-derived memory B cells showing premutated Igs. The results presented herein further weaken this bona fide association because B cells expressing surface IgG, but not CD27, were found in human blood. Representing 1–4% of all peripheral B cells and ∼25% of the IgG+ blood B cells, this population expressed mutated IgG genes showing antigenic selection characteristics but with lower mutation frequencies than that of CD27+IgG+ B cells. However, their morphology and phenotype were similar to that of CD27+IgG+ cells. Interestingly, the proportion of IgG2 over IgG3 transcripts was opposite in CD27−IgG+ and CD27+IgG+ cells, suggesting distinct functions or origins. Overall, these findings extend the memory B cell reservoir beyond the CD27+ compartment and could provide further insights into B cell disorders of unknown etiology.

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“…In animal models, vIL6, like hIL6, acts as a multifunctional cytokine and promotes plasmacytosis, angiogenesis and haematopoiesis 94. The effects of vIL6 are through its direct interaction with CD130/gp-130, the signal transducer of the IL6 receptor complex 95 96. In fact, vIL6 activates all of the known hIL6-induced signalling pathways, including the JAK-STAT and RAS-MAP kinase signalling cascades 92.…”

Section: Role Of Kshv In Lymphomagenesismentioning

confidence: 99%

Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 and lymphoproliferative disorders

Bacon

2007

J Clin Pathol

113

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Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), is a recent addition to the list of human viruses that are directly associated with lymphoproliferative disorders. KSHV was first shown to be involved in multicentric Castleman disease and primary effusion lymphoma (PEL). Subsequently, the virus was identified in solid lymphomas, often of extranodal sites, with morphological and immunophenotypic characteristics similar to those of PEL, and in other lymphoproliferative disorders with heterogeneous clinicopathological presentations. The recent advances in our understanding of the histology, immunophenotype and pathogenesis of these KSHV-associated lymphoproliferative disorders are reviewed.

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Viral Interleukin 6 Stimulates Human Peripheral Blood B Cells That Are Unresponsive to Human Interleukin 6

Cited by 19 publications

References 38 publications

Identification of novel SNPs in the interleukin 6 receptor gene (IL6R)

Identification of novel SNPs in the interleukin 6 receptor gene (IL6R)

A New Memory CD27−IgG+ B Cell Population in Peripheral Blood Expressing VH Genes with Low Frequency of Somatic Mutation

Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 and lymphoproliferative disorders

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