scholarly journals Antigen-specific, MHC nonrestricted T helper cell-induced B cell activation.

1986 ◽  
Vol 164 (5) ◽  
pp. 1773-1778 ◽  
Author(s):  
S M Friedman ◽  
J A Jover ◽  
E K Chartash ◽  
M K Crow

We used a cloned, TNP-specific, MHC-restricted, human Th cell line, E-11, and an assay of cognate Th-B cell interaction, BLAST-2 antigen expression on the B cell surface, to investigate the functional nature of the Th cell antigen receptor. We observed that E-11 induces BLAST-2 expression by resting B cells in a hapten-dependent, hapten-specific, but MHC nonrestricted manner. The implication of these results for the Th cell receptor are discussed.

1982 ◽  
Vol 156 (2) ◽  
pp. 350-360 ◽  
Author(s):  
Y Asano ◽  
M Shigeta ◽  
C G Fathman ◽  
A Singer ◽  
R J Hodes

It has recently been demonstrated that the Lyb-5+ and Lyb-5- B cell subpopulations differ in their requirements for major histocompatibility complex (MHC)-restricted activation by T helper (TH) cells. To determine whether these MHC-restricted and -unrestricted pathways of B cell activation result from differences in the participating TH cell populations or reflect differences exclusively in the responding B cell subpopulations, experiments were carried out using cloned TH cells for in vitro antibody responses to trinitrophenyl-keyhole limpet hemocyanin. The same cloned T helper cells were able to activate both CBA/N (Lyb-5-) B cells and CBA/CaHN (Lyb-5+ + Lyb-5-) B cells under different experimental conditions. The activation of Lyb-5-B cells by cloned T helper cells required both MHC-restricted TH cell-B cell interaction and carrier-hapten linkage. In contrast, the activation of Lyb-5+ B cells required only MHC-restricted T helper cell interaction with accessory cells, while T-B interaction was MHC unrestricted and did not require carrier-hapten linkage. Thus, the differences in activation requirements observed for the Lyb-5- and Lyb-5+ B cell subsets do not result from differences in the TH cell populations activating these B cells, but rather reflect differences in the ability of these B cells to respond to signals from the same TH cells.


2007 ◽  
Vol 178 (3) ◽  
pp. 1468-1476 ◽  
Author(s):  
Elke Scandella ◽  
Katja Fink ◽  
Tobias Junt ◽  
Beatrice M. Senn ◽  
Evelyn Lattmann ◽  
...  

1991 ◽  
Vol 5 (13) ◽  
pp. 2770-2776 ◽  
Author(s):  
Randolph J. Noelle ◽  
E. Charles Snow

Author(s):  
Richard J. Hodes ◽  
Yoshihiro Asano ◽  
Minoru Shigeta ◽  
Karen S. Hathcock ◽  
Masao Kimoto ◽  
...  

1989 ◽  
Vol 121 (1) ◽  
pp. 99-112 ◽  
Author(s):  
Mary K. Crow ◽  
Barbara Kushner ◽  
Juan A. Jover ◽  
Steven M. Friedman ◽  
Susan E. Mechanic ◽  
...  

2005 ◽  
Vol 16 (5) ◽  
pp. 2275-2284 ◽  
Author(s):  
Shengli Hao ◽  
Avery August

Polymerization of the actin cytoskeleton has been found to be essential for B-cell activation. We show here, however, that stimulation of BCR induces a rapid global actin depolymerization in a BCR signal strength-dependent manner, followed by polarized actin repolymerization. Depolymerization of actin enhances and blocking actin depolymerization inhibits BCR signaling, leading to altered BCR and lipid raft clustering, ERK activation, and transcription factor activation. Furthermore actin depolymerization by itself induces altered lipid raft clustering and ERK activation, suggesting that F-actin may play a role in separating lipid rafts and in setting the threshold for cellular activation.


2007 ◽  
Vol 179 (11) ◽  
pp. 7397-7405 ◽  
Author(s):  
Liliana Busconi ◽  
Jason W. Bauer ◽  
Joseph R. Tumang ◽  
Amy Laws ◽  
Kristin Perkins-Mesires ◽  
...  

Blood ◽  
2008 ◽  
Vol 111 (6) ◽  
pp. 3266-3275 ◽  
Author(s):  
Hong Xu ◽  
Jun Yan ◽  
Yiming Huang ◽  
Paula M. Chilton ◽  
Chuanlin Ding ◽  
...  

Abstract Sensitization is a critical unresolved challenge in transplantation. We show for the first time that blockade of CD154 alone or combined with T-cell depletion prevents sensitization. Allogeneic skin grafts were rejected by recipients treated with anti-αβ T-cell receptor (TCR), anti-CD154, anti-OX40L, or anti–inducible costimulatory pathway (ICOS) mAb alone with a kinetic similar to untreated recipients. However, the production of anti–donor MHC antibody was prevented in mice treated with anti-CD154 mAb only, suggesting a specific role for the CD154-CD40 pathway in B-cell activation. The impairment of T cell–dependent B-cell responses by blocking CD154 occurs through inhibiting activation of T and B cells and secretion of IFN-γ and IL-10. Combined treatment with both anti-CD154 and anti–αβ TCR abrogated antidonor antibody production and resulted in prolonged skin graft survival, suggesting the induction of both T- and B-cell tolerance with prevention of allogeneic sensitization. In addition, we show that the tolerance induced by combined treatment was nondeletional. Moreover, these sensitization-preventive strategies promote bone marrow engraftment in recipients previously exposed to donor alloantigen. These findings may be clinically relevant to prevent allosensitization with minimal toxicity and point to humoral immunity as playing a dominant role in alloreactivity in sensitized recipients.


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