scholarly journals Essential role for B cells in transplantation tolerance

2011 ◽  
Vol 23 (5) ◽  
pp. 685-691 ◽  
Author(s):  
Robert R Redfield ◽  
Eduardo Rodriguez ◽  
Ronald Parsons ◽  
Kumar Vivek ◽  
Moiz M Mustafa ◽  
...  
2016 ◽  
Vol 53 ◽  
pp. 75
Author(s):  
Fumio Takizawa ◽  
Zhen Xu ◽  
David Parra ◽  
Daniela Gomez ◽  
Scott LaPatra ◽  
...  

Cell Cycle ◽  
2014 ◽  
Vol 13 (10) ◽  
pp. 1583-1589 ◽  
Author(s):  
Claire Leduc ◽  
Guillaume Chemin ◽  
Nadine Puget ◽  
Carla Sawan ◽  
Mohammed Moutahir ◽  
...  

2003 ◽  
Vol 198 (10) ◽  
pp. 1595-1608 ◽  
Author(s):  
Keiko Fujikawa ◽  
Ana V. Miletic ◽  
Frederick W. Alt ◽  
Roberta Faccio ◽  
Tracie Brown ◽  
...  

The Vav family of Rho guanine nucleotide exchange factors is thought to orchestrate signaling events downstream of lymphocyte antigen receptors. Elucidation of Vav function has been obscured thus far by the expression of three highly related family members. We generated mice lacking all Vav family proteins and show that Vav-null mice produce no functional T or B cells and completely fail to mount both T-dependent and T-independent humoral responses. Whereas T cell development is blocked at an early stage in the thymus, immature B lineage cells accumulate in the periphery but arrest at a late “transitional” stage. Mechanistically, we show that the Vav family is crucial for both TCR and B cell receptor (BCR)–induced Ca2+ signaling and, surprisingly, is only required for mitogen-activated protein kinase (MAPK) activation in developing and mature T cells but not in B cells. Thus, the abundance of immature B cells generated in Vav-null mice may be due to intact Ras/MAPK signaling in this lineage. Although the expression of Vav1 alone is sufficient for normal lymphocyte development, our data also reveal lineage-specific roles for Vav2 and Vav3, with the first demonstration that Vav3 plays a critical compensatory function in T cells. Together, we define an essential role for the entire Vav protein family in lymphocyte development and activation and establish the limits of functional redundancy both within this family and between Vav and other Rho–guanine nucleotide exchange factors.


2004 ◽  
Vol 78 ◽  
pp. 536-537
Author(s):  
S Deng ◽  
M M. Mohiuddin ◽  
X Huang ◽  
D Moore ◽  
E Velidedeoglu ◽  
...  

2011 ◽  
Vol 85 (21) ◽  
pp. 11391-11400 ◽  
Author(s):  
S.-M. Kang ◽  
D.-G. Yoo ◽  
M.-C. Kim ◽  
J.-M. Song ◽  
M.-K. Park ◽  
...  

2020 ◽  
Vol 218 (2) ◽  
Author(s):  
Jeremy F. Brooks ◽  
Julie Zikherman

Although BAFF/BLyS and its receptor, BAFFR, play critical roles in naive B cell survival, the pathways involved in the persistence of memory B cells are largely unknown. In this issue of JEM, two groups, Müller-Winkler et al. (https://doi.org/10.1084/jem.20191393) and Lau et al. (https://doi.org/10.1084/jem.20191167), take complementary approaches to identify an essential role for BAFFR in the survival of memory B cells.


2020 ◽  
Vol 130 (7) ◽  
pp. 3453-3466 ◽  
Author(s):  
Stella H.W. Khiew ◽  
Dharmendra Jain ◽  
Jianjun Chen ◽  
Jinghui Yang ◽  
Dengping Yin ◽  
...  

2012 ◽  
Vol 24 (2) ◽  
pp. 92-95 ◽  
Author(s):  
Andrew B. Adams ◽  
Kenneth A. Newell

2012 ◽  
Vol 24 (2) ◽  
pp. 75-76
Author(s):  
Ali Naji ◽  
Hooman Noorchashm ◽  
Michael P. Cancro

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