Human B Cell Tolerance and Its Failure in Rheumatoid Arthritis.
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| Title: | Human B Cell Tolerance and Its Failure in Rheumatoid Arthritis. |
|---|---|
| Authors: | SAMUELS, JONATHAN1 (AUTHOR), NG, YEN‐SHING1 (AUTHOR), COUPILLAUD, CLAIRE1 (AUTHOR), PAGET, DANIEL1 (AUTHOR), MEFFRE, ERIC1,2 (AUTHOR) |
| Source: | Annals of the New York Academy of Sciences. 2005, Vol. 1062 Issue 1, p116-126. 11p. |
| Subjects: | B cells, Cell receptors, Rheumatoid arthritis, Bone marrow, Immunoglobulins |
| Abstract: | Random V(D)J gene assembly generates many autoreactive B cell receptors (BCRs). In healthy donors, most autoreactive developing B cells are removed either in the bone marrow or in the periphery, revealing two B cell tolerance checkpoints. The regulation and the mechanisms that ensure this human B cell tolerance are poorly characterized, but they require proper BCR signaling. Indeed, patients with X-linked agammaglobulinemia who carry mutations in the BTK gene, which encodes an essential BCR signaling component, fail to establish proper central B cell tolerance, as demonstrated by the release of self-reactive B cells in the periphery. In autoimmune diseases such as rheumatoid arthritis (RA), B cell tolerance is broken and autoantibodies are secreted. Our recent results show that RA patients suffer from defective central and peripheral B cell tolerance checkpoints, which may favor the development of autoimmunity. Also, about half of our RA patients display unusual immunoglobulin light chain repertoires showing impaired secondary recombination regulation, which indicates that receptor editing, one of the mechanisms that normally ensures B cell tolerance, may often be defective in RA. [ABSTRACT FROM AUTHOR] |
| Copyright of Annals of the New York Academy of Sciences is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Engineering Source |
| FullText | Text: Availability: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Human B Cell Tolerance and Its Failure in Rheumatoid Arthritis. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22SAMUELS%2C+JONATHAN%22">SAMUELS, JONATHAN</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22NG%2C+YEN‐SHING%22">NG, YEN‐SHING</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22COUPILLAUD%2C+CLAIRE%22">COUPILLAUD, CLAIRE</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22PAGET%2C+DANIEL%22">PAGET, DANIEL</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22MEFFRE%2C+ERIC%22">MEFFRE, ERIC</searchLink><relatesTo>1,2</relatesTo> (AUTHOR) – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Annals+of+the+New+York+Academy+of+Sciences%22">Annals of the New York Academy of Sciences</searchLink>. 2005, Vol. 1062 Issue 1, p116-126. 11p. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22B+cells%22">B cells</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+receptors%22">Cell receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Rheumatoid+arthritis%22">Rheumatoid arthritis</searchLink><br /><searchLink fieldCode="DE" term="%22Bone+marrow%22">Bone marrow</searchLink><br /><searchLink fieldCode="DE" term="%22Immunoglobulins%22">Immunoglobulins</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Random V(D)J gene assembly generates many autoreactive B cell receptors (BCRs). In healthy donors, most autoreactive developing B cells are removed either in the bone marrow or in the periphery, revealing two B cell tolerance checkpoints. The regulation and the mechanisms that ensure this human B cell tolerance are poorly characterized, but they require proper BCR signaling. Indeed, patients with X-linked agammaglobulinemia who carry mutations in the BTK gene, which encodes an essential BCR signaling component, fail to establish proper central B cell tolerance, as demonstrated by the release of self-reactive B cells in the periphery. In autoimmune diseases such as rheumatoid arthritis (RA), B cell tolerance is broken and autoantibodies are secreted. Our recent results show that RA patients suffer from defective central and peripheral B cell tolerance checkpoints, which may favor the development of autoimmunity. Also, about half of our RA patients display unusual immunoglobulin light chain repertoires showing impaired secondary recombination regulation, which indicates that receptor editing, one of the mechanisms that normally ensures B cell tolerance, may often be defective in RA. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Annals of the New York Academy of Sciences is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1196/annals.1358.014 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 11 StartPage: 116 Subjects: – SubjectFull: B cells Type: general – SubjectFull: Cell receptors Type: general – SubjectFull: Rheumatoid arthritis Type: general – SubjectFull: Bone marrow Type: general – SubjectFull: Immunoglobulins Type: general Titles: – TitleFull: Human B Cell Tolerance and Its Failure in Rheumatoid Arthritis. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: SAMUELS, JONATHAN – PersonEntity: Name: NameFull: NG, YEN‐SHING – PersonEntity: Name: NameFull: COUPILLAUD, CLAIRE – PersonEntity: Name: NameFull: PAGET, DANIEL – PersonEntity: Name: NameFull: MEFFRE, ERIC IsPartOfRelationships: – BibEntity: Dates: – D: 05 M: 12 Text: 2005 Type: published Y: 2005 Identifiers: – Type: issn-print Value: 00778923 Numbering: – Type: volume Value: 1062 – Type: issue Value: 1 Titles: – TitleFull: Annals of the New York Academy of Sciences Type: main |
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