scholarly journals Self-Antigens Displayed on Liposomal Nanoparticles above a Threshold of Epitope Density Elicit Class-Switched Autoreactive Antibodies Independent of T Cell Help

2019 ◽  
Vol 204 (2) ◽  
pp. 335-347 ◽  
Author(s):  
Zhilin Chen ◽  
Wei-Yun Wholey ◽  
Alireza Hassani Najafabadi ◽  
James J. Moon ◽  
Irina Grigorova ◽  
...  
Keyword(s):  
T Cell ◽  
Autoreactive Antibodies ◽  
Epitope Density ◽  
Liposomal Nanoparticles ◽  
T Cell Help ◽  
Self Antigens

scholarly journals CD4+ T Cell Help Impairs CD8+ T Cell Deletion Induced by Cross-presentation of Self-Antigens and Favors Autoimmunity

1997 ◽  
Vol 186 (12) ◽  
pp. 2057-2062 ◽  
Author(s):  
Christian Kurts ◽  
Francis R. Carbone ◽  
Megan Barnden ◽  
Effrossini Blanas ◽  
Janette Allison ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cell ◽  
Cd4 T Cell ◽  
T Cell Tolerance ◽  
Presentation Of Self ◽  
Cross Presentation ◽  
Cd4 T Cell Help ◽  
T Cell Help ◽  
Self Antigens

Self-antigens expressed in extrathymic tissues such as the pancreas can be transported to draining lymph nodes and presented in a class I–restricted manner by bone marrow-derived antigen-presenting cells. Such cross-presentation of self-antigens leads to CD8+ T cell tolerance induction via deletion. In this report, we investigate the influence of CD4+ T cell help on this process. Small numbers of autoreactive OVA-specific CD8+ T cells were unable to cause diabetes when adoptively transferred into mice expressing ovalbumin in the pancreatic β cells. Coinjection of OVA-specific CD4+ helper T cells, however, led to diabetes in a large proportion of mice (68%), suggesting that provision of help favored induction of autoimmunity. Analysis of the fate of CD8+ T cells indicated that CD4+ T cell help impaired their deletion. These data indicate that control of such help is critical for the maintenance of CD8+ T cell tolerance induced by cross-presentation.

scholarly journals A brief history of T cell help to B cells

2015 ◽  
Vol 15 (3) ◽  
pp. 185-189 ◽  
Author(s):  
Shane Crotty
Keyword(s):  
T Cell ◽  
B Cells ◽  
History Of ◽  
T Cell Help

scholarly journals Cd40-Independent Pathways of T Cell Help for Priming of Cd8+ Cytotoxic T Lymphocytes

2000 ◽  
Vol 191 (3) ◽  
pp. 541-550 ◽  
Author(s):  
Zhengbin Lu ◽  
Lingxian Yuan ◽  
Xianzheng Zhou ◽  
Eduardo Sotomayor ◽  
Hyam I. Levitsky ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Cytotoxic T Lymphocyte ◽  
Cell Communication ◽  
Cd8 T Cell ◽  
Cd4 Help ◽  
T Cell Help

In many cases, induction of CD8+ CTL responses requires CD4+ T cell help. Recently, it has been shown that a dominant pathway of CD4+ help is via antigen-presenting cell (APC) activation through engagement of CD40 by CD40 ligand on CD4+ T cells. To further study this three cell interaction, we established an in vitro system using dendritic cells (DCs) as APCs and influenza hemagglutinin (HA) class I and II peptide–specific T cell antigen receptor transgenic T cells as cytotoxic T lymphocyte precursors and CD4+ T helper cells, respectively. We found that CD4+ T cells can provide potent help for DCs to activate CD8+ T cells when antigen is provided in the form of either cell lysate, recombinant protein, or synthetic peptides. Surprisingly, this help is completely independent of CD40. Moreover, CD40-independent CD4+ help can be documented in vivo. Finally, we show that CD40-independent T cell help is delivered through both sensitization of DCs and direct CD4+–CD8+ T cell communication via lymphokines. Therefore, we conclude that CD4+ help comprises at least three components: CD40-dependent DC sensitization, CD40-independent DC sensitization, and direct lymphokine-dependent CD4+–CD8+ T cell communication.

scholarly journals Definition of conditions that enable antigen-specific activation of the majority of isolated trinitrophenol-binding B cells.

1982 ◽  
Vol 156 (6) ◽  
pp. 1635-1649 ◽  
Author(s):  
J C Cambier ◽  
J G Monroe ◽  
M J Neale
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
Interleukin 1 ◽  
Isolated Cells ◽  
Cellular Events ◽  
Accessory Cells ◽  
B Cell Growth Factor ◽  
Human Gamma Globulin ◽  
Definition Of ◽  
T Cell Help

In an effort to further elucidate the early cellular events in generation of antibody responses, we have determined the requirements for antigen-specific initiation of the G0 to G1 transition by isolated trinitrophenol (TNP) -binding B lymphocytes. TNP-binding cells were isolated from normal B6D2F1 splenocyte populations using hapten affinity fractionation on disulfide-bonded TNP-gelatin-coated plates. Populations prepared in this way are greater than or equal to 96% immunoglobulin positive and 70-95% antigen binding. Isolated cells were cultured for 48 h in the presence of a variety of TNP conjugates including TNP-Brucella abortus (Ba), TNP-Ficoll, TNP-sheep erythrocytes (SRBC), TNP-human gamma globulin (HGG), or TNP-ovalbumin (OVA) before being harvested and subjected to acridine orange cell cycle analysis. As many as 80% of cells were in cycle by 48 h in response to TNP-Ba, a thymus-independent (TI1 antigen. A smaller proportion (congruent to 40%) were in cycle in response to TNP-Ficoll, a TI2 antigen. Significant activation was not detected in cultures challenged with the thymus-dependent immunogens TNP-SRBC, TNP-HGG, and TNP-OVA. Addition of interleukin 1 (IL-1), IL-2, B cell growth factor, and/or T cell-replacing factor to cultures did not facilitate responses to these immunogens, suggesting a requirement for antigen-specific T cell help for entry into cell cycle induced by thymus dependent antigens. Activation by TNP-Ba was antigen specific and independent of accessory cells, occurring with equal efficiency in bulk and single-cell cultures. Activation by TNP-Ba was inhibitable by anti-Fab and anti-mu antibodies, but not by anti-delta antibodies. Results indicate that activation of TNP-binding cells to enter cell cycle by TNP-Ba is independent of accessory cells and requires interaction of antigen with cell surface IgM. Exposure to thymus-dependent TNP-immunogens plus nonspecific helper factors is insufficient to cause entry of TNP-binding cells into cycle.

Immune Responses to Retinal Self-Antigens in CD25+CD4+Regulatory T-Cell–Depleted Mice

2004 ◽  
Vol 45 (6) ◽  
pp. 1879 ◽  
Author(s):  
Masaru Takeuchi ◽  
Hiroshi Keino ◽  
Takeshi Kezuka ◽  
Masahiko Usui ◽  
Osamu Taguchi
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Regulatory T Cell ◽  
Self Antigens

scholarly journals B cell activation by cytomegalovirus.

1983 ◽  
Vol 158 (6) ◽  
pp. 2171-2176 ◽  
Author(s):  
L M Hutt-Fletcher ◽  
N Balachandran ◽  
M H Elkins
Keyword(s):  
T Cell ◽  
B Cell ◽  
Virus Replication ◽  
Human Cytomegalovirus ◽  
Cell Response ◽  
Cell Activation ◽  
B Cell Activation ◽  
T Cell Help ◽  
Cell Activator ◽  
B Cell Response

Human cytomegalovirus is shown to be a nonspecific polyclonal B cell activator. The B cell response is independent of virus replication and requires little, if any, T cell help.

Sign in / Sign up

Export Citation Format

Share Document