scholarly journals Epinephrine-primed murine bone marrow-derived dendritic cells facilitate production of IL-17A and IL-4 but not IFN-γ by CD4+ T cells

2010 ◽  
Vol 24 (7) ◽  
pp. 1126-1136 ◽  
Author(s):  
Byung-Jin Kim ◽  
Harlan P. Jones
2005 ◽  
Vol 101 (2) ◽  
pp. 193-201 ◽  
Author(s):  
Shorena Janelidze ◽  
Karin Enell ◽  
Edward Visse ◽  
Anna Darabi ◽  
Leif G. Salford ◽  
...  

2011 ◽  
Vol 188 (3) ◽  
pp. 1168-1177 ◽  
Author(s):  
Xiongfei Xu ◽  
Hai Yi ◽  
Zhenhong Guo ◽  
Cheng Qian ◽  
Sheng Xia ◽  
...  

2009 ◽  
Vol 182 (6) ◽  
pp. 3372-3379 ◽  
Author(s):  
Vincent Lombardi ◽  
Laurence Van Overtvelt ◽  
Stéphane Horiot ◽  
Philippe Moingeon

2014 ◽  
Vol 20 (2) ◽  
pp. 192-201 ◽  
Author(s):  
Elizabeth O. Stenger ◽  
Brian R. Rosborough ◽  
Lisa R. Mathews ◽  
Huihui Ma ◽  
Markus Y. Mapara ◽  
...  

2014 ◽  
Vol 162 (1) ◽  
pp. 188-199 ◽  
Author(s):  
Jaris Valencia ◽  
Víctor G. Martínez ◽  
Laura Hidalgo ◽  
Carmen Hernández-López ◽  
Noelia M. Canseco ◽  
...  

2020 ◽  
Vol 94 (13) ◽  
Author(s):  
Christiane S. Eberhardt ◽  
Andreas Wieland ◽  
Tahseen H. Nasti ◽  
Alba Grifoni ◽  
Elizabeth Wilson ◽  
...  

ABSTRACT Childhood immunization with the live-attenuated varicella-zoster virus (VZV) vaccine induces protective immune responses. Routine VZV vaccination started only 2 decades ago, and thus, there are few studies examining the longevity of vaccine-induced immunity. Here, we analyzed the quantity of VZV-specific plasma cells (PCs) and CD4 T cells in the bone marrow (BM) of healthy young adults (n = 15) following childhood VZV immunization. Long-lived BM resident plasma cells constitutively secrete antibodies, and we detected VZV-specific PCs in the BM of all subjects. Anti-VZV plasma antibody titers correlated positively with the number of VZV-specific BM PCs. Furthermore, we quantified the number of interferon gamma (IFN-γ)-producing CD4 T cells specific for VZV glycoprotein E and all other structural and nonstructural VZV proteins in both BM and blood (peripheral blood mononuclear cells [PBMCs]). The frequency of VZV-specific IFN-γ-producing CD4 T cells was significantly higher in PBMCs than BM. Our study shows that VZV-specific PCs and VZV-specific CD4 memory T cells persist up to 20 years after vaccination. These findings indicate that childhood VZV vaccination can elicit long-lived immune memory responses in the bone marrow. IMPORTANCE Childhood varicella-zoster virus (VZV) immunization induces immune memory responses that protect against primary VZV infection, chicken pox. In the United States, routine childhood VZV vaccination was introduced only 2 decades ago. Hence, there is limited information on the longevity of B and CD4 T cell memory, which are both important for protection. Here, we showed in 15 healthy young adults that VZV-specific B and CD4 T cell responses are detectable in bone marrow (BM) and blood up to 20 years after vaccination. Specifically, we measured antibody-secreting plasma cells in the BM and VZV-specific CD4 T cells in BM and blood. These findings suggest that childhood VZV vaccination induces long-lived immunity.


2015 ◽  
Vol 17 (4) ◽  
pp. 275-284 ◽  
Author(s):  
Elizabeth Liu ◽  
Jennifer Van Grol ◽  
Carlos S. Subauste

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2004-2004
Author(s):  
Sarah Morin-Zorman ◽  
Christian Wysocki ◽  
Edwina Kisanga ◽  
David Gonzalez ◽  
David Rothstein ◽  
...  

Abstract Graft-versus-host disease (GVHD) limits the broader application of allogeneic hematopoietic stem cell transplantation. In prior studies we defined roles for both host and donor-derived antigen presenting cells (APCs) in the activation of alloreactive donor T cells and promotion of GVHD. While initial T cell activation in GVHD occurs predominantly in secondary lymphoid organs (SLO), we have consistently observed MHCII+ donor-derived tissue APCs (t-APCs), including tissue dendritic cells (t-DCs) in histopathologic GVHD lesions, frequently adjacent to infiltrating T cells. We hypothesize that productive interactions occur between donor APCs and T cells in situ in GVHD target tissues, which propagate disease locally. We could not use knockout or APC depletion approaches to study T cell: t-APCs interactions as they impact APCs systemically and might therefore affect T cell stimulation in SLO. We therefore utilized two-photon intravital microscopy to analyze interactions between fluorescent donor CD4+ T cells and t-DCs in skin. 129 (H-2b) hosts were irradiated and reconstituted with B6 (H-2b) CD11c-YFP transgenic (Tg) Bone Marrow (BM) with B6 RFP Tg CD4 cells and nonfluorescent B6 CD8 cells. We imaged ear skin in GVHD mice 4 weeks later. In general CD4 cells co-localized with DCs. We observed CD4+ T cells that were highly motile and only in transient contact with DCs and others that made stable contact with DCs. To determine how much TCR: MHCII interactions drive sustained CD4+ T cell: DC interactions and arrest CD4+ T cell motility, mice were imaged and then injected with an MHCII blocking antibody (Ab; Y3P) with continued imaging of the same regions. After injection, T cell mean speed significantly increased and the proportion of T cells in stable contact with DCs decreased, indicating that transient disruption of TCR: MHCII is sufficient to restore motility to some T cells. In a second approach to assess the specificity of CD4+ T cell: t-DC interactions we transplanted 129 mice with B6 RFP+ CD4 cells, nonfluorescent CD8 cells and a mix of CD11c-YFP MHCII-/- and RFP wt BM or a mix of CD11c-YFP wt and RFP Tg MHCII-/- BM. We are currently comparing the motility of CD4 cells that make contact with MHCII+ as compared to MHCII- DCs, with the prediction that contact times will be shorter with the latter. Our data suggest that CD4+ T cells make cognate interactions with t-DCs in skin and we hypothesize that these interactions promote GVHD locally. Because the graft-versus-leukemia effect occurs primarily in bone marrow and secondary lymphoid tissues, targeting of tissue-infiltrating APCs could represent a unique strategy to ameliorate GVHD while preserving GVL. Disclosures: No relevant conflicts of interest to declare.


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