T Cell Clonal Anergy

2015 ◽  
pp. 92-116 ◽  
Author(s):  
Kathleen M. Gilbert
Keyword(s):  
T Cell ◽  
Clonal Anergy

scholarly journals Immune Tolerance Split between Hepatitis B Virus Precore and Core Proteins

2005 ◽  
Vol 79 (5) ◽  
pp. 3016-3027 ◽  
Author(s):  
Margaret Chen ◽  
Matti Sällberg ◽  
Janice Hughes ◽  
Joyce Jones ◽  
Luca G. Guidotti ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
T Cell ◽  
Hepatitis B ◽  
Cell Receptor ◽  
T Cell Tolerance ◽  
Cell Tolerance ◽  
Clonal Deletion ◽  
Core Proteins ◽  
B Virus ◽  
Clonal Anergy

ABSTRACT The function of the hepatitis B virus (HBV) precore or HBeAg is largely unknown because it is not required for viral assembly, infection, or replication. However, the HBeAg does appear to play a role in viral persistence. It has been suggested that the HBeAg may promote HBV chronicity by functioning as an immunoregulatory protein. As a model of chronic HBeAg exposure and to examine the tolerogenic potential of the HBV precore and core (HBcAg) proteins, HBc/HBeAg-transgenic (Tg) mice crossed with T cell receptor (TCR)-Tg mice expressing receptors for the HBc/HBeAgs (i.e., TCR-antigen double-Tg pairs) were produced. This study revealed three phenotypes of HBe/HBcAg-specific T-cell tolerance: (i) profound T-cell tolerance most likely mediated by clonal deletion, (ii) T-cell clonal ignorance, and (iii) nondeletional T-cell tolerance mediated by clonal anergy and dependent on the structure, location, and concentration of the tolerogen. The secreted HBeAg is significantly more efficient than the intracellular HBcAg at eliciting T-cell tolerance. The split T-cell tolerance between the HBeAg and the HBcAg and the clonal heterogeneity of HBc/HBeAg-specific T-cell tolerance may have significant implications for natural HBV infection and especially for precore-negative chronic hepatitis.

scholarly journals Clonal anergy induced in a CD8+ hapten-specific cytotoxic T-cell clone by an altered hapten-peptide ligand

Immunology ◽  
2001 ◽  
Vol 102 (1) ◽  
pp. 8-14 ◽  
Author(s):  
T. Preckel ◽  
S Hellwig ◽  
U Pflugfelder ◽  
M. B. Lappin ◽  
H. U. Weltzien
Keyword(s):  
T Cell ◽  
Cell Clone ◽  
Cytotoxic T Cell ◽  
Peptide Ligand ◽  
T Cell Clone ◽  
Clonal Anergy

scholarly journals Immunoglobulin M and D antigen receptors are both capable of mediating B lymphocyte activation, deletion, or anergy after interaction with specific antigen.

1992 ◽  
Vol 176 (4) ◽  
pp. 991-1005 ◽  
Author(s):  
R Brink ◽  
C C Goodnow ◽  
J Crosbie ◽  
E Adams ◽  
J Eris ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
Transgenic Mice ◽  
B Lymphocyte ◽  
Specific Antigen ◽  
Antigen Receptors ◽  
Antigen B ◽  
Self Antigen ◽  
Clonal Anergy

A series of immunoglobulin (Ig)-transgenic mice were generated to study the functional capabilities of the IgM and IgD classes of B lymphocyte antigen receptor in regulating both cellular development and responses to specific antigen. B cells from Ig-transgenic mice expressing either hen-egg lysozyme (HEL)-specific IgM or IgD alone were compared with B cells from mice that coexpressed IgM and IgD of the same anti-HEL specificity. In all three types of Ig-transgenic mice, conventional B cells specific for HEL exhibited exclusion of endogenous Ig expression and matured to populate the usual microenvironments in peripheral lymphoid tissues. These peripheral B cells could be stimulated by HEL through either IgM or IgD antigen receptors to generate T cell dependent antibody production in vivo or to enhance T cell independent proliferative responses to lipopolysaccharide in vitro. Conversely, when HEL was encountered in vivo as a self-antigen, B cells expressing HEL-specific IgM or IgD alone were both rendered tolerant. In each case this occurred by clonal anergy in response to soluble autologous HEL, and clonal deletion when HEL was recognized as a membrane-bound self-antigen. Taken together, these findings indicate that IgM and IgD antigen receptors expressed alone on conventional B cells can support normal differentiation, antigen-dependent activation, and induction of self-tolerance, the only overt difference lying in a greater degree of receptor downregulation for IgM relative to IgD after induction of clonal anergy by soluble HEL.

T cell clonal anergy

1997 ◽  
Vol 9 (3) ◽  
pp. 351-357 ◽  
Author(s):  
Ronald H Schwartz
Keyword(s):  
T Cell ◽  
Clonal Anergy

scholarly journals CD2 is involved in maintenance and reversal of human alloantigen-specific clonal anergy.

1994 ◽  
Vol 180 (5) ◽  
pp. 1665-1673 ◽  
Author(s):  
V A Boussiotis ◽  
G J Freeman ◽  
J D Griffin ◽  
G S Gray ◽  
J G Gribben ◽  
...  
Keyword(s):  
T Cell ◽  
Costimulatory Molecules ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Human Organ ◽  
Leukocyte Antigen ◽  
Cell Clones ◽  
B7 Family ◽  
Clonal Anergy

Induction and maintenance of a state of T cell unresponsiveness to specific alloantigen would have significant implications for human organ transplantation. Using human histocompatibility leukocyte antigen DR7-specific helper T cell clones, we demonstrate that blockade of the B7 family of costimulatory molecules is sufficient to induce alloantigen-specific T cell clonal anergy. Anergized cells do not respond to alloantigen and a variety of costimulatory molecules, including B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1), and lymphocyte function-associated molecule (LFA)-3. However, after culture in exogenous interleukin (IL)-2 for at least 7 d, anergized cells can respond to alloantigen in the presence of LFA-3. LFA-3 costimulation subsequently restores responsiveness to alloantigen in the presence of previously insufficient costimulatory signals. Expression of CD2R epitope is downregulated on anergic cells and is restored after 7 d of IL-2 culture. The loss of the CD2R is temporally associated with the inability of anergized cells to respond to LFA-3. These results suggest that in addition to blockade of B7 family members, inhibition of CD2 and, potentially, other costimulatory pathways that might reverse anergy will be necessary to maintain prolonged alloantigen-specific tolerance.

Constitutive active p21ras enhances primary T cell responsiveness to Ca2+ signals without interfering with the induction of clonal anergy

2002 ◽  
Vol 32 (9) ◽  
pp. 2500-2509 ◽  
Author(s):  
Daniela Crespi ◽  
Stefania Massa ◽  
Veronica Basso ◽  
Sara Colombetti ◽  
Daniel L. Mueller ◽  
...  
Keyword(s):  
T Cell ◽  
Clonal Anergy
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