دورية أكاديمية
TLR2, TLR4 and the MyD88 signaling are crucial for the in vivo generation and the longevity of long-lived antibody-secreting cells.
العنوان: | TLR2, TLR4 and the MyD88 signaling are crucial for the in vivo generation and the longevity of long-lived antibody-secreting cells. |
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المؤلفون: | Komegae EN; Immunoregulation Unit, Special Laboratory of Applied Toxinology, Butantan Institute and Department of Immunology, University of São Paulo, São Paulo, Brazil., Grund LZ, Lopes-Ferreira M, Lima C |
المصدر: | PloS one [PLoS One] 2013 Aug 05; Vol. 8 (8), pp. e71185. Date of Electronic Publication: 2013 Aug 05 (Print Publication: 2013). |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: Electronic-Print Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: San Francisco, CA : Public Library of Science |
مواضيع طبية MeSH: | Antibody-Producing Cells/*physiology , Cell Differentiation/*genetics , Myeloid Differentiation Factor 88/*physiology , Toll-Like Receptor 2/*physiology , Toll-Like Receptor 4/*physiology, Animals ; Cell Differentiation/immunology ; Cell Survival/genetics ; Cell Survival/immunology ; Cells, Cultured ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Signal Transduction/genetics ; Signal Transduction/immunology |
مستخلص: | This study was undertaken to gain better insights into the role of TLRs and MyD88 in the development and differentiation of memory B cells, especially of ASC, during the Th2 polarized memory response induced by Natterins. Our in vivo findings demonstrated that the anaphylactic IgG1 production is dependent on TLR2 and MyD88 signaling, and that TLR4 acts as adjuvant accelerating the synthesis of high affinity-IgE. Also, TLR4 (MyD88-independent) modulated the migration of innate-like B cells (B1a and B2) out of the peritoneal cavity, and the emigration from the spleen of B1b and B2 cells. TLR4 (MyD88-independent) modulated the emigration from the spleen of Bmem as well as ASC B220(pos). TLR2 triggered to the egress from the peritoneum of Bmem (MyD88-dependent) and ASC B220(pos) (MyD88-independent). We showed that TLR4 regulates the degree of expansion of Bmem in the peritoneum (MyD88-dependent) and in BM (MyD88-independent) as well as of ASC B220(neg) in the spleen (MyD88-independent). TLR2 regulated the intensity of the expansion of Bmem (MyD88-independent) and ASC B220(pos) (MyD88-dependent) in BM. Finally, TLR4 signals sustained the longevity of ASC B220(pos) (MyD88-independent) and ASC B220(neg) into the peritoneum (MyD88-dependent) and TLR2 MyD88-dependent signaling supported the persistence of B2 cells in BM, Bmem in the spleen and ASC B220(neg) in peritoneum and BM. Terminally differentiated ASC B220(neg) required the cooperation of both signals through TLR2/TLR4 via MyD88 for longevity in peritoneum, whereas Bmem required only TLR2/MyD88 to stay in spleen, and ASC B220(pos) rested in peritoneum dependent on TLR4 signaling. Our data sustain that earlier events on memory B cells differentiation induced in secondary immune response against Natterins, after secondary lymph organs influx and egress, may be the key to determining peripheral localization of innate-like B cells and memory B cells as ASC B220(pos) and ASC B220(neg). |
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المشرفين على المادة: | 0 (Myd88 protein, mouse) 0 (Myeloid Differentiation Factor 88) 0 (Tlr2 protein, mouse) 0 (Tlr4 protein, mouse) 0 (Toll-Like Receptor 2) 0 (Toll-Like Receptor 4) |
تواريخ الأحداث: | Date Created: 20130814 Date Completed: 20140414 Latest Revision: 20211021 |
رمز التحديث: | 20231215 |
مُعرف محوري في PubMed: | PMC3733974 |
DOI: | 10.1371/journal.pone.0071185 |
PMID: | 23940714 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1932-6203 |
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DOI: | 10.1371/journal.pone.0071185 |