دورية أكاديمية
أعرض في EDS

TLR2, TLR4 and the MyD88 signaling are crucial for the in vivo generation and the longevity of long-lived antibody-secreting cells.

التفاصيل البيبلوغرافية
العنوان: TLR2, TLR4 and the MyD88 signaling are crucial for the in vivo generation and the longevity of long-lived antibody-secreting cells.
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).
References: J Exp Med. 2000 Apr 3;191(7):1149-66. (PMID: 10748233)
Immunol Rev. 2006 Jun;211:269-79. (PMID: 16824134)
Trends Immunol. 2002 Jun;23(6):296-300. (PMID: 12072368)
J Immunol. 2002 Nov 15;169(10):5874-80. (PMID: 12421970)
Cytokine. 2012 Aug;59(2):335-51. (PMID: 22633287)
Immunity. 2007 Aug;27(2):190-202. (PMID: 17723214)
J Exp Med. 2009 Nov 23;206(12):2641-57. (PMID: 19917774)
J Exp Med. 2006 Oct 30;203(11):2541-50. (PMID: 17060475)
J Immunol. 2003 Apr 1;170(7):3819-27. (PMID: 12646649)
J Exp Med. 1998 Nov 2;188(9):1691-703. (PMID: 9802981)
Nature. 2007 Jun 21;447(7147):972-8. (PMID: 17538624)
J Exp Med. 2004 Dec 6;200(11):1491-501. (PMID: 15583019)
Biochem Pharmacol. 2004 Dec 1;68(11):2151-7. (PMID: 15498505)
Immunity. 2005 Jul;23(1):7-18. (PMID: 16039575)
Immunol Rev. 2010 Sep;237(1):117-39. (PMID: 20727033)
Eur J Immunol. 2009 Aug;39(8):2065-75. (PMID: 19637202)
Nature. 1970 Aug 15;227(5259):680-5. (PMID: 5432063)
J Immunol. 2007 Jun 15;178(12):7779-86. (PMID: 17548615)
Mol Cell Biol. 2002 Jul;22(13):4771-80. (PMID: 12052884)
Life Sci. 1969 Aug 15;8(16):813-20. (PMID: 5306608)
J Immunol. 2008 Aug 1;181(3):1746-52. (PMID: 18641311)
Nat Immunol. 2001 Aug;2(8):675-80. (PMID: 11477402)
Eur J Immunol. 2011 Mar;41(3):588-91. (PMID: 21341259)
Semin Immunol. 2009 Aug;21(4):185-93. (PMID: 19502082)
J Immunol. 1958 Oct;81(4):355-7. (PMID: 13588003)
Immunity. 2004 Jul;21(1):81-93. (PMID: 15345222)
Eur J Immunol. 2001 Feb;31(2):350-9. (PMID: 11180098)
Genes Dev. 1998 Jul 1;12(13):1953-61. (PMID: 9649500)
Nat Rev Immunol. 2009 Aug;9(8):535-42. (PMID: 19556980)
Nat Immunol. 2004 Sep;5(9):943-52. (PMID: 15300245)
J Exp Med. 2002 Mar 18;195(6):737-45. (PMID: 11901199)
Curr Top Microbiol Immunol. 2000;252:163-9. (PMID: 11125473)
J Exp Med. 1994 Jul 1;180(1):111-21. (PMID: 8006578)
PLoS One. 2007 Sep 12;2(9):e863. (PMID: 17848994)
Nat Rev Immunol. 2012 Mar 16;12(4):282-94. (PMID: 22421786)
Biochimie. 2006 Jun;88(6):693-9. (PMID: 16488069)
Immunity. 2011 May 27;34(5):637-50. (PMID: 21616434)
Nat Immunol. 2003 Sep;4(9):920-7. (PMID: 12925853)
J Exp Med. 2009 Aug 31;206(9):1971-82. (PMID: 19687229)
J Immunol. 2005 Mar 15;174(6):3173-7. (PMID: 15749846)
Ann Rheum Dis. 2008 Dec;67 Suppl 3:iii87-9. (PMID: 19022822)
Cytokine. 1999 Jun;11(6):389-99. (PMID: 10346978)
Nat Immunol. 2008 Apr;9(4):369-77. (PMID: 18345001)
Toxicon. 2006 Oct;48(5):499-508. (PMID: 16930659)
Science. 2002 Apr 12;296(5566):298-300. (PMID: 11951031)
Immunology. 2012 Aug;136(4):370-9. (PMID: 22444240)
Ann Rheum Dis. 2001 Nov;60 Suppl 3:iii6-12. (PMID: 11890657)
Blood. 2003 Jun 1;101(11):4500-4. (PMID: 12560217)
J Immunol. 2002 Sep 1;169(5):2507-15. (PMID: 12193720)
Nature. 2002 Apr 11;416(6881):603-7. (PMID: 11948342)
Nat Rev Immunol. 2005 Mar;5(3):230-42. (PMID: 15738953)
Immunity. 2002 Jul;17(1):51-62. (PMID: 12150891)
Biochimie. 2005 Aug;87(8):687-99. (PMID: 16054523)
Nat Rev Immunol. 2005 Jun;5(6):446-58. (PMID: 15928677)
J Exp Med. 2001 Jul 2;194(1):45-56. (PMID: 11435471)
Annu Rev Immunol. 2005;23:367-86. (PMID: 15771575)
Nat Immunol. 2006 Jul;7(7):773-82. (PMID: 16767092)
Nature. 2005 Nov 17;438(7066):364-8. (PMID: 16292312)
Immunity. 2003 Oct;19(4):607-20. (PMID: 14563324)
Nat Immunol. 2004 Jul;5(7):713-20. (PMID: 15184895)
Nature. 2001 Jul 19;412(6844):300-7. (PMID: 11460154)
Nat Immunol. 2012 Feb 26;13(4):396-404. (PMID: 22366892)
Infect Immun. 2001 Mar;69(3):1477-82. (PMID: 11179315)
Nat Immunol. 2008 Mar;9(3):310-8. (PMID: 18300366)
Cell Regul. 1989 Nov;1(1):27-35. (PMID: 2519615)
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
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0071185