scholarly journals Cbls boost B cells

2020 ◽  
Vol 217 (9) ◽  
Author(s):  
Michelle A. Linterman

T cell regulation of antibody-mediated immunity is critical for health. In this issue of JEM, Li et al. (https://doi.org/10.1084/jem.20191537) identify the Cbl family of E3 ubiquitin ligases as B cell–intrinsic gatekeepers of T cell–dependent humoral immunity.

2021 ◽  
Vol 433 (1) ◽  
pp. 166685 ◽  
Author(s):  
Motoki Horii ◽  
Takashi Matsushita

1981 ◽  
Vol 153 (1) ◽  
pp. 1-12 ◽  
Author(s):  
P K Mongini ◽  
K E Stein ◽  
W E Paul

The effect of T lymphocytes on the IgM, IgG3, IgG1, IgG2b, and IgG2a responses of B lymphocytes to the type-2 T-independent antigens, trinitrophenylated (TNP)-Ficoll, and TNP-Levan, was investigated. T cell-bearing nu/+ mice were found to produce substantially higher IgG2 serum anti-TNP antibody than their athymic counterparts, and nu/nu and nu/+ IgG2a titers exhibiting more disparity than nu/nu and nu/+ IgG2b titers. The Igm, IgG3, and IgG1 anti-TNP levels in nu/nu and nu/+ mice were indistinguishable. By cell transfer experiments, it was determined that this variance in nude and heterozygote IgG2 responses could not be explained by B cell differences between the two strains or by suppressive effects on IgG2 production within nu/nu mice. Rather, the difference was shown to be the result of the absence of T cells at the time B cells were responding to antigen. In the absence of T cells, the strength of the nu/nu anti-TNP antibody response was found to be in the following order: IgM > IgG3 > IgG1 > IgG2b > IgG2a, a heirarchy identical with the recently proposed heavy chain gene order. The possibilities that T cells influence IgG2 production via their specific recognition of IgG2-bearing B cells or via signals to increase heavy chain switching of responding B cell clones are discussed.


1991 ◽  
Vol 34 (3) ◽  
pp. 291-297 ◽  
Author(s):  
R. HUCHET ◽  
D. GRANDJON ◽  
O. HALLE-PANNENKO

Blood ◽  
2002 ◽  
Vol 100 (13) ◽  
pp. 4557-4564 ◽  
Author(s):  
Thomas J. Waldschmidt ◽  
Angela Panoskaltsis-Mortari ◽  
Ronald T. McElmurry ◽  
Lorraine T. Tygrett ◽  
Patricia A. Taylor ◽  
...  

In allogeneic hematopoietic stem cell transplant recipients, restoration of humoral immunity is delayed and can remain impaired for years. In many severe combined immune deficiency (SCID) patients given haploidentical bone marrow (BM), lesions in humoral immunity are exacerbated by poor engraftment of donor B cells. The nature of these defects is important to understand as they render patients susceptible to infection. Previous work in mice suggested that in utero transplantation (IUT) of allogeneic BM might offer several advantages for the correction of primary immune deficiencies. In SCID mice given fully allogeneic BM in utero, the lymphoid compartment was restored with minimal evidence of graft-versus-host disease (GVHD). The present report examines B-cell reconstitution and function in mice that have received allogeneic IUT. Results are compared with those of adult mice given total body irradiation (TBI) followed by transplantation with allogeneic BM. In addition to enumerating the various B-cell subsets present in BM, spleen, and peritoneal cavity (PC), B-cell competence was assessed by challenging mice with T cell–independent (TI) and T cell–dependent (TD) antigens. The results demonstrated that all B-cell subsets in the BM and periphery were restored in allogeneic IUT and TBI mice, as were antibody responses after TI challenge. Upon immunization with TD antigens, however, IUT and TBI mice exhibited suboptimal responses as measured by the capacity to isotype switch and generate germinal center (GC) B cells. Thus, although allogeneic BM transplantation results in complete recovery of the B-cell compartment, certain elements of the humoral response remain defective.


1999 ◽  
Vol 117 (5) ◽  
pp. 1105-1112 ◽  
Author(s):  
Mario M. D'Elios ◽  
Amedeo Amedei ◽  
Marta Manghetti ◽  
Francesco Costa ◽  
Cosima T. Baldari ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document