scholarly journals T cell anergy in perinatal mice is promoted by T reg cells and prevented by IL-33

2019 ◽  
Vol 216 (6) ◽  
pp. 1328-1344 ◽  
Author(s):  
Jonatan Tuncel ◽  
Christophe Benoist ◽  
Diane Mathis
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
High Expression ◽  
T Cell Anergy ◽  
Tissue Antigens ◽  
Cell Anergy ◽  
Deficient Mice

Perinatal T cells broadly access nonlymphoid tissues, where they are exposed to sessile tissue antigens. To probe the outcome of such encounters, we examined the defective elimination of self-reactive clones in Aire-deficient mice. Nonlymphoid tissues were sequentially seeded by distinct waves of CD4+ T cells. Early arrivers were mostly Foxp3+ regulatory T (T reg) cells and metabolically active, highly proliferative conventional T cells (T conv cells). T conv cells had unusually high expression of PD-1 and the IL-33 receptor ST2. As T conv cells accumulated in the tissue, they gradually lost expression of ST2, ceased to proliferate, and acquired an anergic phenotype. The transition from effector to anergic state was substantially faster in ST2-deficient perinates, whereas it was abrogated in IL-33–treated mice. A similar dampening of anergy occurred after depletion of perinatal T reg cells. Attenuation of anergy through PD-1 blockade or IL-33 administration promoted the immediate breakdown of tolerance and onset of multiorgan autoimmunity. Hence, regulating IL-33 availability may be critical in maintaining T cell anergy.

scholarly journals Interleukin-10 induces a long-term antigen-specific anergic state in human CD4+ T cells.

1996 ◽  
Vol 184 (1) ◽  
pp. 19-29 ◽  
Author(s):  
H Groux ◽  
M Bigler ◽  
J E de Vries ◽  
M G Roncarolo
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
T Cell Anergy ◽  
Factor Alpha ◽  
Cell Anergy ◽  
Anergic T Cells ◽  
Macrophage Colony

Human CD4+ T cells, activated by allogeneic monocytes in a primary mixed lymphocyte reaction in the presence of exogenous interleukin (IL) 10, specifically failed to proliferate after restimulation with the same alloantigens. A comparable state of T cell unresponsiveness could be induced by activation of CD4+ T cells by cross-linked anti-CD3 monoclonal antibodies (mAbs) in the presence of exogenous IL-10. The anergic T cells failed to produce IL-2, IL-5, IL-10, interferon gamma, tumor necrosis factor alpha, and granulocyte/macrophage colony-stimulating factor. The IL-10-induced anergic state was long-lasting. T cell anergy could not be reversed after restimulation of the cells with anti-CD3 and anti-CD28 mAbs, although CD3 and CD28 expression was normal. In addition, restimulation of anergized T cells with anti-CD3 mAbs induced normal Ca2+ fluxes and resulted in increased CD3, CD28, and class II major histocompatibility complex expression, indicating that calcineurin-mediated signaling occurs in these anergic cells. However, the expression of the IL-2 receptor alpha chain was not upregulated, which may account for the failure of exogenous IL-2 to reverse the anergic state. Interestingly, anergic T cells and their nonanergic counterparts showed comparable levels of proliferation and cytokine production after activation with phorbol myristate acetate and Ca2+ ionophore, indicating that a direct activation of a protein kinase C-dependent pathway can overcome the tolerizing effect of IL-10. Taken together, these data demonstrate that IL-10 induces T cell anergy and therefore may play an important role in the induction and maintenance of antigen-specific T cell tolerance.

T1212 Upregulation of E3 Ubiquitin Ligases Related to T Cell Anergy in CD4+ T Cells Isolated from Patients with Ulcerative Colitis in Remission

2008 ◽  
Vol 134 (4) ◽  
pp. A-508
Author(s):  
Satoshi Egawa ◽  
Hideki Iijima ◽  
Shinichiro Shinzaki ◽  
Sachiko Nakajima ◽  
Jumpei Kondo ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Ubiquitin Ligases ◽  
E3 Ubiquitin Ligases ◽  
T Cell Anergy ◽  
Cell Anergy

scholarly journals Relative Resistance in the Development of T Cell Anergy in CD4+T Cells from Simian Immunodeficiency Virus Disease-Resistant Sooty Mangabeys

2001 ◽  
Vol 166 (1) ◽  
pp. 506-516 ◽  
Author(s):  
Pavel Bostik ◽  
Ann E. Mayne ◽  
Francois Villinger ◽  
Kenneth P. Greenberg ◽  
Jonathan D. Powell ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Simian Immunodeficiency Virus ◽  
Cd4 T Cells ◽  
Virus Disease ◽  
Relative Resistance ◽  
T Cell Anergy ◽  
Immunodeficiency Virus ◽  
Sooty Mangabeys ◽  
Cell Anergy

Interaction of Retinal Pigmented Epithelial Cells and CD4 T Cells Leads to T-Cell Anergy

2007 ◽  
Vol 48 (10) ◽  
pp. 4654 ◽  
Author(s):  
Dale S. Gregerson ◽  
Neal D. Heuss ◽  
Kathleen L. Lew ◽  
Scott W. McPherson ◽  
Deborah A. Ferrington
Keyword(s):  
T Cells ◽  
T Cell ◽  
Epithelial Cells ◽  
Cd4 T Cells ◽  
T Cell Anergy ◽  
Cell Anergy ◽  
Retinal Pigmented Epithelial Cells

scholarly journals 144 T cell anergy regulator Egr2 identifies a quiescent stem-like phenotype in malignant T cells

2017 ◽  
Vol 137 (5) ◽  
pp. S24
Author(s):  
H. Hamidullah ◽  
S. Roy ◽  
A. Anshu ◽  
W. Kittipongdaja ◽  
S.M. Schieke
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Anergy ◽  
Cell Anergy ◽  
Malignant T Cells

scholarly journals Selective anergy of V beta 8+,CD4+ T cells in Staphylococcus enterotoxin B-primed mice.

1990 ◽  
Vol 172 (4) ◽  
pp. 1065-1070 ◽  
Author(s):  
Y Kawabe ◽  
A Ochi
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
T Cell Anergy ◽  
Specific Cytotoxicity ◽  
Enterotoxin B ◽  
Staphylococcus Enterotoxin B

The cellular basis of the in vitro and in vivo T cell responses to Staphylococcus enterotoxin B (SEB) has been investigated. The proliferation and cytotoxicity of V beta 8.1,2+,CD4+ and CD8+ T cells were observed in in vitro response to SEB. In primary cytotoxicity assays, CD4+ T cells from control spleens were more active than their CD8+ counterparts, however, in cells derived from SEB-primed mice, CD8+ T cells were dominant in SEB-specific cytotoxicity. In vivo priming with SEB abrogated the response of V beta 8.1,2+,CD4+ T cells despite the fact that these cells exist in significant number. This SEB-specific anergy occurred only in V beta 8.1,2+,CD4+ T cells but not in CD8+ T cells. These findings indicate that the requirement for the induction of antigen-specific anergy is different between CD4+ and CD8+ T cells in post-thymic tolerance, and the existence of coanergic signals for the induction of T cell anergy is suggested.

1L-10 induces antigen-specific T-cell anergy but no regulatory T cells in children with Egg allergy

2003 ◽  
Vol 111 (2) ◽  
pp. S106-S107
Author(s):  
P.A. Eigenmann ◽  
L. Tropia ◽  
C. Hauser ◽  
C.P. Frossard
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Egg Allergy ◽  
T Cell Anergy ◽  
Cell Anergy

CD40-Activated B-Cell Chronic Lymphocytic Leukemia Cells for Tumor Immunotherapy: Stimulation of Allogeneic Versus Autologous T Cells Generates Different Types of Effector Cells

Blood ◽  
1999 ◽  
Vol 93 (6) ◽  
pp. 1992-2002 ◽  
Author(s):  
Raymund Buhmann ◽  
Annette Nolte ◽  
Doreen Westhaus ◽  
Bertold Emmerich ◽  
Michael Hallek
Keyword(s):  
T Cells ◽  
T Cell ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Tumor Antigens ◽  
Lymphocytic Leukemia ◽  
T Cell Anergy ◽  
Cell Anergy ◽  
Cell Chronic Lymphocytic Leukemia ◽  
Stimulation Of

Although spontaneous remissions may rarely occur in B-cell chronic lymphocytic leukemia (B-CLL), T cells do generally not develop a clinically significant response against B-CLL cells. Because this T-cell anergy against B-CLL cells may be caused by the inability of B-CLL cells to present tumor-antigens efficiently, we examined the possibility of upregulating critical costimulatory (B7-1 and B7-2) and adhesion molecules (ICAM-1 and LFA-3) on B-CLL cells to improve antigen presentation. The stimulation of B-CLL cells via CD40 by culture on CD40L expressing feeder cells induced a strong upregulation of costimulatory and adhesion molecules and turned the B-CLL cells into efficient antigen-presenting cells (APCs). CD40-activated B-CLL (CD40-CLL) cells stimulated the proliferation of both CD4+ and CD8+ T cells. Interestingly, stimulation of allogeneic versus autologous T cells resulted in the expansion of different effector populations. Allogeneic CD40-CLL cells allowed for the expansion of specific CD8+cytolytic T cells (CTL). In marked contrast, autologous CD40-CLL cells did not induce a relevant CTL response, but rather stimulated a CD4+, Th1-like T-cell population that expressed high levels of CD40L and released interferon-γ in response to stimulation by CD40-CLL cells. Together, these results support the view that CD40 activation of B-CLL cells might reverse T-cell anergy against the neoplastic cell clone, although the character of the immune response depends on the major histocompatibility complex (MHC) background on which the CLL or tumor antigens are presented. These findings may have important implications for the design of cellular immunotherapies for B-CLL.

Sign in / Sign up

Export Citation Format

Share Document