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Plos One : Tlr2, Tlr4 and the Myd88 Signaling Are Crucial for the in Vivo Generation and the Longevity of Long-lived Antibody-secreting Cells, Volume 8

By Richard, Yolande

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Book Id: WPLBN0003968733
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Reproduction Date: 2015

Title: Plos One : Tlr2, Tlr4 and the Myd88 Signaling Are Crucial for the in Vivo Generation and the Longevity of Long-lived Antibody-secreting Cells, Volume 8  
Author: Richard, Yolande
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection
Historic
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Publisher: Plos

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Richard, Y. (n.d.). Plos One : Tlr2, Tlr4 and the Myd88 Signaling Are Crucial for the in Vivo Generation and the Longevity of Long-lived Antibody-secreting Cells, Volume 8. Retrieved from http://netlibrary.net/


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Description : 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 innatelike 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 B220pos. TLR2 triggered to the egress from the peritoneum of Bmem (MyD88-dependent) and ASC B220pos (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 B220neg in the spleen (MyD88-independent). TLR2 regulated the intensity of the expansion of Bmem (MyD88-independent) and ASC B220pos (MyD88-dependent) in BM. Finally, TLR4 signals sustained the longevity of ASC B220pos (MyD88- independent) and ASC B220neg into the peritoneum (MyD88-dependent) and TLR2 MyD88-dependent signaling supported the persistence of B2 cells in BM, Bmem in the spleen and ASC B220neg in peritoneum and BM. Terminally differentiated ASC B220neg 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 B220pos 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 innatelike B cells and memory B cells as ASC B220pos and ASC B220neg.

 

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