Taci Is a Traf-Interacting Receptor for Tall-1, a Tumor Necrosis Factor Family Member Involved in B Cell Regulation

Xia, Xing-Zhong; Treanor, James; Senaldi, Giorgio; Khare, Sanjay D.; Boone, T.; Kelley, Michael J.; Theill, Lars E.; Colombero, Anne; Solovyev, Irina; Lee, Frances; McCabe, Susan; Elliott, Robin; Miner, Kent; Hawkins, Nessa; Guo, Jane; Stolina, Marina; Yu, Gang; Wang, Judy; Delaney, John; Meng, Shi-Yuan; Boyle, William J.; Hsu, Hailing

doi:10.1084/jem.192.1.137

Cited by 236 publications

(186 citation statements)

References 20 publications

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“…The data were consistent with previous reports (19,22,23) and showed that, over time, the primary anti-NP response was significantly reduced with BAFF inhibition when compared with control animals (Fig. 4).…”

Section: Discussionsupporting

confidence: 82%

Cutting Edge: Germinal Centers Formed in the Absence of B Cell-Activating Factor Belonging to the TNF Family Exhibit Impaired Maturation and Function

Vora

Wang

Rao

et al. 2003

The Journal of Immunology

132

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Germinal centers (GCs) form in B cell follicles and require specific signals for development and maintenance. B cell-activating factor belonging to the TNF family (BAFF) is a fundamental B cell survival factor and therefore may influence GC reactions and subsequent Ab responses. To test this possibility, the effect of BAFF neutralization in immunized mice was assessed. Using B cell maturation Ag-Fc, we demonstrate that BAFF blockade does not inhibit GC formation or somatic hypermutation. However, GCs in B cell maturation Ag-Fc-treated mice dissipated more rapidly than those of control mice and did not form a mature follicular dendritic cell reticulum. Examination of immunized BAFF-null mice validated the BAFF-independent nature of GC formation. Furthermore, Ab responses, including high-affinity responses, were attenuated. This is the first evidence that BAFF is required for maintenance, but not initiation, of the GC reaction, and it further hints that somatic hypermutation within the GC and selection of Ag-specific high-affinity Ab could be uncoupled.

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Section: Discussionsupporting

confidence: 82%

Cutting Edge: Germinal Centers Formed in the Absence of B Cell-Activating Factor Belonging to the TNF Family Exhibit Impaired Maturation and Function

Vora

Wang

Rao

et al. 2003

The Journal of Immunology

132

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“…3). These data are consistent with previous observations that TRAF3 interacts with TACI, but not BCMA, in mammalian overexpression systems (10,13).…”

Section: Traf3 Is Recruited To Baff-r By Tall-1 Stimulationsupporting

confidence: 83%

TNFR-Associated Factor-3 Is Associated With BAFF-R and Negatively Regulates BAFF-R-Mediated NF-κB Activation and IL-10 Production

Shu

2002

The Journal of Immunology

138

126

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TALL-1 is a member of the TNF family that is critically involved in B cell survival, maturation, and progression of lupus-like autoimmune diseases. TALL-1 has three receptors, including BCMA, TACI, and BAFF-R, which are mostly expressed by B lymphocytes. Gene knockout studies have indicated that BAFF-R is the major stimulatory receptor for TALL-1 signaling and is required for normal B cell development. The intracellular signaling mechanisms of BAFF-R are not known. In this report, we attempted to identify BAFF-R-associated downstream proteins by yeast two-hybrid screening. This effort identified TNFR-associated factor (TRAF)3 as a protein specifically interacting with BAFF-R in yeast two-hybrid assays. Coimmunoprecipitation experiments indicated that BAFF-R interacts with TRAF3 in B lymphoma cells and this interaction is stimulated by TALL-1 treatment. Domain mapping experiments indicated that both a 6-aa membrane proximal region and the C-terminal 35 aa of BAFF-R are required for its interaction with TRAF3. Moreover, overexpression of TRAF3 inhibits BAFF-R-mediated NF-κB activation and IL-10 production. Taken together, our findings suggest that TRAF3 is a negative regulator of BAFF-R-mediated NF-κB activation and IL-10 production.

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“…The R202H mutation is located in the part of the receptor interacting with the calciummodulator and cyclophilin ligand. 26 The binding of APRIL and BAFF induces class switch recombination. 8,9 It is suggested that TACI is involved in the class switch recombination to both IgA and IgG in humans.…”

Section: Discussionmentioning

confidence: 99%

Rare mutations in TNFRSF13B increase the risk of asthma symptoms in Swedish children

et al. 2011

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TACI (transmembrane activator and calcium modulator and cyclophilin ligand interactor) mutations seem to be associated with autoimmunity and common variable immunodeficiency in humans. Because of its role in immune responses, we investigated the association between TACI mutations and infection proneness/asthma symptoms in children. A total of 2372 children were genotyped for TACI mutations (I87N, C104R, S144X, A181E, R202H and ins204A). Serum IgA, IgG and specific IgE levels were determined in children with mutations. Data on parentally reported allergic diseases and infections were collected. In all, 55 individuals with TACI mutations were identified. Children with TACI mutations had a 2-fold increased risk of wheeze at 2 and 4 years of age and a 2.5-fold increased risk of asthma was seen at 4 years of age. None of the children with mutations suffered from IgA deficiency (o0.07 g l À1 ). No significant differences in serum IgG levels or specific IgE were found. Common variants in asthma susceptibility genes may account for up to 40% of cases of childhood-onset asthma, indicating a high contribution, compared with other common disorders. The role of rare variants/mutations in the pathogenesis of asthma is less clear. We conclude that mutations in TACI are the contributing factors for asthma symptoms in Swedish children, although the mechanisms still remain elusive.

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Taci Is a Traf-Interacting Receptor for Tall-1, a Tumor Necrosis Factor Family Member Involved in B Cell Regulation

Cited by 236 publications

References 20 publications

Cutting Edge: Germinal Centers Formed in the Absence of B Cell-Activating Factor Belonging to the TNF Family Exhibit Impaired Maturation and Function

Cutting Edge: Germinal Centers Formed in the Absence of B Cell-Activating Factor Belonging to the TNF Family Exhibit Impaired Maturation and Function

TNFR-Associated Factor-3 Is Associated With BAFF-R and Negatively Regulates BAFF-R-Mediated NF-κB Activation and IL-10 Production

Rare mutations in TNFRSF13B increase the risk of asthma symptoms in Swedish children

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