ArticleThe Journal of experimental medicine2016
Impairment on the lateral mobility induced by structural changes underlies the functional deficiency of the lupus-associated polymorphism FcγRIIB-T232.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed.
- INPP5K limits PtdIns (4,5)P2 accumulation in CD19 microclusters and restrains CD19 co-receptor membrane proximity and BCR-proximal signaling in B cells.Frontiers in immunology · 2026Article
- The STING inhibitor (ISD-017) reduces glomerulonephritis in 129.B6.Fcgr2b-deficient mice.Scientific reports · 2024Article
- Identification and characterization of novel genetic variants in the first Chinese family of mucopolysaccharidosis IIIC (Sanfilippo C syndrome).Journal of cellular and molecular medicine · 2024Article
- Physical-Chemical Regulation of Membrane Receptors Dynamics in Viral Invasion and Immune Defense.Journal of molecular biology · 2023Review
- FcγRIIB regulates autoantibody responses by limiting marginal zone B cell activation.The Journal of clinical investigation · 2022Article
- WASP family proteins regulate the mobility of the B cell receptor during signaling activation.Nature communications · 2020Article
- Article
- Fc receptor-like 1 intrinsically recruits c-Abl to enhance B cell activation and function.Science advances · 2019Article
- Article
- The Post-GWAS Era: How to Validate the Contribution of Gene Variants in Lupus.Current rheumatology reports · 2019Review
- IgG and Fcγ Receptors in Intestinal Immunity and Inflammation.Frontiers in immunology · 2019Review
- The Human FcγRII (CD32) Family of Leukocyte FcR in Health and Disease.Frontiers in immunology · 2019Review
- Transmembrane domain dependent inhibitory function of FcγRIIB.Protein & cell · 2018Review
- The Lupus-Associated Fcγ Receptor IIb-I232T Polymorphism Results in Impairment in the Negative Selection of Low-Affinity Germinal Center B Cells Via c-Abl in Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2018Article
- IgG3 regulates tissue-like memory B cells in HIV-infected individuals.Nature immunology · 2018Article
- PI(4,5)P2 determines the threshold of mechanical force-induced B cell activation.The Journal of cell biology · 2018Article
- Cytoskeletal control of B cell responses to antigens.Nature reviews. Immunology · 2017Review
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22 authors.
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Abstract
FcγRIIB functions to suppress the activation of immune cells. A single-nucleotide polymorphism in the transmembrane (TM) domain of FcγRIIB, FcγRIIB-T232, is associated with lupus. In this study, we investigated the pathogenic mechanism of FcγRIIB-T232 at both functional and structural levels. Our results showed that FcγRIIB-T232 exhibited significantly reduced lateral mobility compared with FcγRIIB-I232 and was significantly less enriched into the microclusters of immune complexes (ICs) after stimulation. However, if sufficient responding time is given for FcγRIIB-T232 to diffuse and interact with the ICs, FcγRIIB-T232 can restore its inhibitory function. Moreover, substituting the FcγRIIB-T232 TM domain with that of a fast floating CD86 molecule restored both the rapid mobility and the inhibitory function, which further corroborated the importance of fast mobility for FcγRIIB to function. Mechanistically, the crippled lateral mobility of FcγRIIB-T232 can be explained by the structural changes of the TM domain. Both atomistic simulations and nuclear magnetic resonance measurement indicated that the TM helix of FcγRIIB-T232 exhibited a more inclined orientation than that of FcγRIIB-I232, thus resulting in a longer region embedded in the membrane. Therefore, we conclude that the single-residue polymorphism T232 enforces the inclination of the TM domain and thereby reduces the lateral mobility and inhibitory functions of FcγRIIB.
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