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Eric Meffre
Yale University
AntibodyNaive B cellImmunologyB cellBiology
105Publications
34H-index
6,181Citations
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Publications 112
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#1Marcel Kuhny (Yale University)H-Index: 1
#2Lisa R. Forbes (BCM: Baylor College of Medicine)H-Index: 16
Last. I. Celine Hanson (BCM: Baylor College of Medicine)H-Index: 25
view all 21 authors...
Patients with common variable immunodeficiency associated with autoimmune cytopenias (CVID+AIC) generate few isotype-switched B cells with severely decreased frequencies of somatic hypermutations (SHM) but their underlying molecular defects remain poorly characterized. We identified a CVID+AIC patient who displays a rare homozygous missense M466V mutation in the beta catenin-like protein 1 (CTNNBL1). Since CTNNBL1 binds activation-induced cytidine deaminase (AID) that catalyzes SHM, we tested AI...
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#1Kofi A. Mensah (Yale University)H-Index: 7
#2Jeff W. Chen (Yale University)H-Index: 2
Last. Eric Meffre (Yale University)H-Index: 34
view all 13 authors...
Patients with rheumatoid arthritis (RA) may display atypical CD21−/lo B cells in their blood, but the implication of this observation remains unclear. We report here that the group of patients with RA and elevated frequencies of CD21−/lo B cells shows decreased ataxia telangiectasia–mutated (ATM) expression and activation in B cells compared with other patients with RA and healthy donor controls. In agreement with ATM involvement in the regulation of V(D)J recombination, patients with RA who sho...
2 CitationsSource
#1Jae-Woong Lee (City of Hope National Medical Center)H-Index: 5
#2Kohei Kume (City of Hope National Medical Center)
Last. Markus Müschen (City of Hope National Medical Center)H-Index: 46
view all 25 authors...
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#1Teresa Sadras (City of Hope National Medical Center)H-Index: 1
#2Mickael Martin (CNRS: Centre national de la recherche scientifique)H-Index: 14
Last. Markus Müschen (City of Hope National Medical Center)H-Index: 46
view all 18 authors...
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#1Eric Meffre (Yale University)H-Index: 34
#2Kevin C. O’Connor (Yale University)H-Index: 38
: A role for B cells in autoimmune diseases is now clearly established both in mouse models and humans by successful treatment of multiple sclerosis and rheumatoid arthritis with anti-CD20 monoclonal antibodies that eliminate B cells. However, the underlying mechanisms by which B cells promote the development of autoimmune diseases remain poorly understood. Here, we review evidence that patients with autoimmune disease suffer from defects in early B-cell tolerance checkpoints and therefore fail ...
4 CitationsSource
#1Nina K. Serwas (Austrian Academy of Sciences)H-Index: 8
#2Birgit Hoeger (Community College of Rhode Island)H-Index: 4
Last. Kaan BoztugH-Index: 31
view all 42 authors...
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#1Theodore L. RothH-Index: 10
#2Cristina Puig-SausH-Index: 5
Last. Alexander MarsonH-Index: 20
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#1Yannick Dieudonné (CNRS: Centre national de la recherche scientifique)H-Index: 1
#2Vincent Gies (UDS: University of Strasbourg)H-Index: 3
Last. Anne-Sophie Korganow (UDS: University of Strasbourg)H-Index: 18
view all 14 authors...
Abstract Systemic lupus (SLE) is characterized by a break of B cell tolerance that plays a central role in disease pathophysiology. An early checkpoint defect occurs at the transitional stage leading to the survival of autoreactive B cells and consequently the production of pathogenic autoantibodies. The main purpose of our work was to determine whether transitional B cells, as the most immature naive B cell subset upstream of pathogenic B cells, display specific features compared to healthy non...
2 CitationsSource
#1Nina K. Serwas (Austrian Academy of Sciences)H-Index: 8
#2Birgit Hoeger (Community College of Rhode Island)H-Index: 4
Last. Kaan BoztugH-Index: 31
view all 42 authors...
Immune responses need to be controlled tightly to prevent autoimmune diseases, yet underlying molecular mechanisms remain partially understood. Here, we identify biallelic mutations in three patients from two unrelated families in differentially expressed in FDCP6 homolog (DEF6) as the molecular cause of an inborn error of immunity with systemic autoimmunity. Patient T cells exhibit impaired regulation of CTLA-4 surface trafficking associated with reduced functional CTLA-4 availability, which is...
4 CitationsSource
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