scholarly journals IgG Opsonization of HIV Impedes Provirus Formation in and Infection of Dendritic Cells and Subsequent Long-Term Transfer to T Cells

2007 ◽  
Vol 178 (12) ◽  
pp. 7840-7848 ◽  
Author(s):  
Doris Wilflingseder ◽  
Zoltan Banki ◽  
Eduardo Garcia ◽  
Monika Pruenster ◽  
Gerald Pfister ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells

scholarly journals Cross-Priming Dendritic Cells Exacerbate Immunopathology after Ischemic Tissue Damage in the Heart

Circulation ◽  
2020 ◽  
Author(s):  
Elvira Forte ◽  
Bryant Perkins ◽  
Amalia Sintou ◽  
Harkaran S. Kalkat ◽  
Angelos Papanikolaou ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cardiac Function ◽  
Functional Decline ◽  
Ischemic Injury ◽  
Myocardial Damage ◽  
Autoimmune Response ◽  
High Dose ◽  
Immune Mediated

Background: Ischemic heart disease is a leading cause of heart failure and despite advanced therapeutic options, morbidity and mortality rates remain high. Although acute inflammation in response to myocardial cell death has been extensively studied, subsequent adaptive immune activity and anti-heart autoimmunity may also contribute to the development of HF. After ischemic injury to the myocardium, dendritic cells (DC) respond to cardiomyocyte necrosis, present cardiac antigen to T cells and potentially initiate a persistent autoimmune response against the heart. Cross-priming DC have the ability to activate both CD4+ helper and CD8 + cytotoxic T cells in response to necrotic cells and may thus be crucial players in exacerbating autoimmunity targeting the heart. This study investigates a role for cross-priming DC in post-MI myocardial impairment through presentation of self-antigen from necrotic cardiomyocytes to cytotoxic CD8 + T cells. Methods: We induced type-2 myocardial infarction (MI)-like ischemic injury in the heart by treatment with a single high dose of the beta-adrenergic agonist isoproterenol. We characterized the DC population in the heart and mediastinal lymph nodes and analyzed long-term cardiac immunopathology and functional decline in wild type and Clec9a -depleted mice lacking DC cross-priming function. Results: A diverse DC population, including cross-priming DC, is present in the heart and activated after ischemic injury. Clec9a -/- mice deficient in DC cross-priming are protected from long-term immune-mediated myocardial damage and decline of cardiac function, likely due to dampened activation of cytotoxic CD8 + T cells. Conclusions: Activation of cytotoxic CD8 + T cells by cross-priming DC contributes to exacerbation of post-ischemic inflammatory damage of the myocardium and corresponding decline in cardiac function. Importantly, this provides novel therapeutic targets to prevent immune-mediated worsening of post-ischemic HF.

scholarly journals Effector memory CD4+ T-cells and dendritic cells are noninvasive biomarkers of late cellular rejection after kidney transplantation

2018 ◽  
Vol 10 (3) ◽  
pp. 207-216 ◽  
Author(s):  
A. V. Nosik ◽  
S. V. Korotkov ◽  
V. V. Smol'nikova ◽  
V. Yu. Grinevich ◽  
D. Yu. Efimov ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Kidney Transplantation ◽  
Kidney Transplant ◽  
Immune Reaction ◽  
Effector Memory ◽  
Absolute Count ◽  
Myeloid Dendritic Cells ◽  
Cellular Rejection

Introduction. Diagnosis of the kidney transplant cellular rejection in the long-term after transplantation remains a challenge. Usual surrogate markers are not enough sensitive and specific. Rejection is an immune reaction to donor alloantigens. The kidney transplant biopsy to diagnose a dysfunction is an invasive procedure with the incidence of complications about 12.6% and can lead to transplant loss. In this regard, the search of immunological biomarkers for early noninvasive and accurate diagnosis of kidney transplant rejection is an actual task.Material and methods. This is a report of the observational retrospective single-center, comparative case-control study in two groups involving 44 patients who underwent kidney transplantation. The first group (REJ) included the patients with the chronic graft dysfunction caused by a biopsy-confirmed late cellular rejection (22 patients). The second group (STA) included the recipients who had no dysfunction in the posttransplant period (22 patients). Flow cytometry of peripheral blood cells was performed to identify immunophenotyping markers of late cellular rejection after kidney transplantation (we determined subpopulations of T, B lymphocytes, and dendritic cells).Results. As a result of our work, we found significant differences in the absolute count of effector memory T cells making 0.147 (0.115–0.260) × 109 cell/L in REJ group, and 0.106 (0.067–0.136) × 109 cell/L in STA group (р = 0.0167).  Relative and absolute counts of myeloid dendritic cells were also different between the groups: 0.65 (0.36–0.73) vs. 1.05 (0.67–1.4) % and 0.039 (0.028–0.056) vs. 0.063 (0.049–0.076) × 109 cell/L, respectively (р = 0.0009, р = 0.003). The numbers of plasmacytoid dendritic cells were also different between the study groups: 0.0038 (0.0021–0.0054) vs. 0.005 (0.0035–0.007) × 109 cell/L for an absolute count (р = 0.0414), and 0.055 (0.04–0.085) vs. 0.09 (0.05–0.12) % for a relative count (р = 0.0197).Conclusion. The obtained data showed that the blood level of dendritic cells, which are the main “professional” initiators of immune reaction, and the level of effector helper T memory cells, which constitute the main lymphocyte subpopulation posing a destructive impact on the kidney transplant, can be considered as diagnostic markers of kidney transplant cellular rejection in the long-term after surgery.

scholarly journals Monotherapy With Anti-CD70 Antibody Causes Long-Term Mouse Cardiac Allograft Acceptance With Induction of Tolerogenic Dendritic Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Jing Zhao ◽  
Weitao Que ◽  
Xiaoxiao Du ◽  
Masayuki Fujino ◽  
Naotsugu Ichimaru ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Allograft Rejection ◽  
Lymphocyte Activation ◽  
Third Party ◽  
Cytotoxic T Cell ◽  
Term Survival ◽  
Cardiac Allografts

Allograft rejection has been an obstacle for the long-term survival of patients. CD70, a tumor necrosis factor (TNF) family member critically expressed on antigen-presenting cells and strongly but transiently up-regulated during lymphocyte activation, represents an important co-stimulatory molecule that induces effective T cell responses. We used a mouse heterotopic cardiac transplantation model to evaluate the effects of monotherapy with the antibody targeting mouse CD70 (FR70) on transplantation tolerance and its immunoregulatory activity. FR70-treated C3H recipient mice permanently accepted B6 fully mismatched cardiac allografts. Consistent with the graft survival, the infiltration of CD8+ T cells in the graft was reduced, dendritic cells were differentiated into a tolerogenic status, and the number of regulatory T cells was elevated both in the graft and the recipient’s spleen. In addition, naïve C3H given an adoptive transfer of spleen cells from the primary recipients with FR70 treatment accepted a heart graft from a matching B6 donor but not third-party BALB/c mice.　Our findings show that treatment with FR70 induced regulatory cells and inhibited cytotoxic T cell proliferation, which led to long-term acceptance of mouse cardiac allografts. These findings highlight the potential role of anti-CD70 antibodies as a clinically effective treatment for allograft rejection.

scholarly journals Infection of Dendritic Cells (DCs), Not DC-SIGN-Mediated Internalization of Human Immunodeficiency Virus, Is Required for Long-Term Transfer of Virus to T Cells

2006 ◽  
Vol 80 (6) ◽  
pp. 2949-2957 ◽  
Author(s):  
Laura Burleigh ◽  
Pierre-Yves Lozach ◽  
Cécile Schiffer ◽  
Isabelle Staropoli ◽  
Valérie Pezo ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Target Cells ◽  
Viral Fusion ◽  
Cell Infection ◽  
Immunodeficiency Virus ◽  
Intracellular Storage

ABSTRACT The C-type lectin DC-SIGN expressed on immature dendritic cells (DCs) captures human immunodeficiency virus (HIV) particles and enhances the infection of CD4+ T cells. This process, known as trans-enhancement of T-cell infection, has been related to HIV endocytosis. It has been proposed that DC-SIGN targets HIV to a nondegradative compartment within DCs and DC-SIGN-expressing cells, allowing incoming virus to persist for several days before infecting target cells. In this study, we provide several lines of evidence suggesting that intracellular storage of intact virions does not contribute to HIV transmission. We show that endocytosis-defective DC-SIGN molecules enhance T-cell infection as efficiently as their wild-type counterparts, indicating that DC-SIGN-mediated HIV internalization is dispensable for trans-enhancement. Furthermore, using immature DCs that are genetically resistant to infection, we demonstrate that several days after viral uptake, HIV transfer from DCs to T cells requires viral fusion and occurs exclusively through DC infection and transmission of newly synthesized viral particles. Importantly, our results suggest that DC-SIGN participates in this process by cooperating with the HIV entry receptors to facilitate cis-infection of immature DCs and subsequent viral transfer to T cells. We suggest that such a mechanism, rather than intracellular storage of incoming virus, accounts for the long-term transfer of HIV to CD4+ T cells and may contribute to the spread of infection by DCs.

scholarly journals Human dendritic cells sequentially matured with CD4+ T cells as a secondary signal favor CTL and long-term T memory cell responses

2012 ◽  
Vol 45 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Thomas Simon ◽  
Séverine Tanguy-Royer ◽  
Pierre-Joseph Royer ◽  
Nicolas Boisgerault ◽  
Jihane Frikeche ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Memory Cell ◽  
Cell Responses ◽  
Human Dendritic Cells

scholarly journals Long-Term Productive Human Immunodeficiency Virus Infection of CD1a-Sorted Myeloid Dendritic Cells

2005 ◽  
Vol 79 (1) ◽  
pp. 602-608 ◽  
Author(s):  
Sergei Popov ◽  
Agnès-Laurence Chenine ◽  
Andreas Gruber ◽  
Pei-Lin Li ◽  
Ruth M. Ruprecht
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Dendritic Cells ◽  
Virus Infection ◽  
Infectious Virus ◽  
Myeloid Dendritic Cells ◽  
Activated T Cells ◽  
Immunodeficiency Virus ◽  
Virus Strains

ABSTRACT Myeloid, CD1a-sorted dendritic cells (MDC) productively replicated human immunodeficiency virus strains encoding envelope genes of either primary X4R5 or R5 strains for up to 45 days. Cell-free supernatant collected from long-term infected MDC, which had been exposed to an X4R5 virus 45 days earlier, was still infectious when placed over activated T cells. These data imply that DC can act as a persistent reservoir of infectious virus.

Ex vivo priming for long-term maintenance of antileukemia human cytotoxic T cells suggests a general procedure for adoptive immunotherapy

Blood ◽  
2001 ◽  
Vol 98 (12) ◽  
pp. 3359-3366 ◽  
Author(s):  
Daniela Montagna ◽  
Rita Maccario ◽  
Franco Locatelli ◽  
Vittorio Rosti ◽  
Young Yang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Dendritic Cells ◽  
Bone Marrow Transplantation ◽  
Adoptive Immunotherapy ◽  
Marrow Transplantation ◽  
Ex Vivo ◽  
Definition Of ◽  
Term Maintenance

Abstract Adoptive cellular immunotherapy has proven to be a successful approach in preventing and curing cytomegalovirus infection and Epstein-Barr virus–associated lymphomas after bone marrow transplantation. Translation of this approach for preventing leukemia relapse after bone marrow transplantation might require ex vivo priming and long-term maintenance of leukemia blast-specific T cells. To accomplish this goal, procedures were optimized for the in vitro priming of naive CD8 using dendritic cells activated by CD40 ligation, interleukin-12 (IL-12), and IL-7. Using T lymphocytes and dendritic cells obtained from HLA-matched allogeneic bone marrow transplantation donors and leukemia blasts as a source of tumor antigens, anti–acute myeloid leukemia cytotoxic T lymphocytes (CTLs) were induced. In these experiments, it was found that though it is possible to induce CTLs using immature dendritic cells, IL-12, and IL-7, obtaining long-term CTLs requires the presence of CD4 T cells in the priming phase. Using this approach, long-term antileukemia CTL lines could be generated from 4 of 4 bone marrow donors. Because this procedure does not require definition of the target antigen and because it selects responding cells from a virgin T-cell repertoire, its general application is suggested in adoptive immunotherapy and in the definition of tumor rejection antigens.

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