scholarly journals Antigen-Specific Tissue-Resident Memory T Cells in the Respiratory System Were Generated following Intranasal Vaccination of Mice with BCG

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Qiongli Wu ◽  
Shuangpeng Kang ◽  
Jun Huang ◽  
Shunqiao Wan ◽  
Binyan Yang ◽  
...  
Keyword(s):  
T Cells ◽  
Nasal Mucosa ◽  
Respiratory System ◽  
Memory T Cells ◽  
Effector Memory ◽  
Effector Memory T Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Specific Tissue ◽  
Resident Memory T Cells

Tissue-resident memory T cells (TRM) are different from effector memory T cells (TEM) and central memory T cells (TCM) and contribute to the protective immunity against local challenges. Currently, we found that CD4+ and CD8+ TRM cells in the nasal mucosa, trachea, lungs, and lavage fluids were heterogeneous on the expression of CD69 and CD103 as well as the production of cytokines including IFN-γ, IL-2, and TNF-α. After intranasal vaccination of mice with BCG, respiratory tissues expressed higher levels of the chemokine CXCL16 and TRM cells expressed CXCR6 to CXCL16. In addition, antigen-specific CD4+ and CD8+ TRM cells expressed cytokines following the stimulation with BCG and persisted in the nasal mucosa, trachea, and lungs for more than a hundred days. At the same time, mice were infected intranasally with live BCG and the results showed that vaccinated mice cleared up live BCG faster than nonvaccinated mice in the respiratory system. Taken together, our data demonstrated that intranasal vaccination of mice with BCG could induce antigen-specific CD4+ and CD8+ TRM cells in the respiratory system and have the ability to provide protection against pulmonary reinfection.

scholarly journals Predominance of heterosubtypic IFN-γ-only-secreting effector memory T cells in pandemic H1N1 naive adults

2012 ◽  
Vol 42 (11) ◽  
pp. 2913-2924 ◽  
Author(s):  
Saranya Sridhar ◽  
Shaima Begom ◽  
Alison Bermingham ◽  
Thedi Ziegler ◽  
Kim L. Roberts ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Effector Memory ◽  
Pandemic H1n1 ◽  
Effector Memory T Cells ◽  
Ifn Γ

A role for interleukin-12/23 in the maturation of human natural killer and CD56+ T cells in vivo

Blood ◽  
2008 ◽  
Vol 111 (10) ◽  
pp. 5008-5016 ◽  
Author(s):  
Sophie Guia ◽  
Céline Cognet ◽  
Ludovic de Beaucoudrey ◽  
Marlowe S. Tessmer ◽  
Emmanuelle Jouanguy ◽  
...  
Keyword(s):  
T Cells ◽  
Nk Cells ◽  
Natural Killer ◽  
Nk Cell ◽  
Memory T Cells ◽  
Effector Memory ◽  
Similar Data ◽  
Effector Memory T Cells ◽  
Ifn Γ

Abstract Natural killer (NK) cells have been originally defined by their “naturally occurring” effector function. However, only a fraction of human NK cells is reactive toward a panel of prototypical tumor cell targets in vitro, both for the production of interferon-γ (IFN-γ) and for their cytotoxic response. In patients with IL12RB1 mutations that lead to a complete IL-12Rβ1 deficiency, the size of this naturally reactive NK cell subset is diminished, in particular for the IFN-γ production. Similar data were obtained from a patient with a complete deficit in IL-12p40. In addition, the size of the subset of effector memory T cells expressing CD56 was severely decreased in IL-12Rβ1– and IL-12p40–deficient patients. Human NK cells thus require in vivo priming with IL-12/23 to acquire their full spectrum of functional reactivity, while T cells are dependent upon IL-12/23 signals for the differentiation and/or the maintenance of CD56+ effector memory T cells. The susceptibility of IL-12/23 axis–deficient patients to Mycobacterium and Salmonella infections in combination with the absence of mycobacteriosis or salmonellosis in the rare cases of human NK cell deficiencies point to a role for CD56+ T cells in the control of these infections in humans.

scholarly journals A repertoire-independent and cell-intrinsic defect in murine GVHD induction by effector memory T cells

Blood ◽  
2011 ◽  
Vol 118 (23) ◽  
pp. 6209-6219 ◽  
Author(s):  
Kathryn W. Juchem ◽  
Britt E. Anderson ◽  
Cuiling Zhang ◽  
Jennifer M. McNiff ◽  
Anthony J. Demetris ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Effector Memory ◽  
Intrinsic Defect ◽  
Intrinsic Properties ◽  
Graft Versus Host ◽  
Effector Memory T Cells ◽  
Alloreactive T Cells ◽  
Donor T Cells ◽  
Ifn Γ

Abstract Effector memory T cells (TEM) do not cause graft-versus-host disease (GVHD), though why this is has not been elucidated. To compare the fates of alloreactive naive (TN) or memory (TM) T cells, we developed a model of GVHD in which donor T cells express a transgene-encoded TCR specific for an antigenic peptide that is ubiquitously expressed in the recipient. Small numbers of naive TCR transgenic (Tg) T cells induced a robust syndrome of GVHD in transplanted recipients. We then used an established method to convert TCR Tg cells to TM and tested these for GVHD induction. This allowed us to control for the potentially different frequencies of alloreactive T cells among TN and TM, and to track fates of alloreactive T cells after transplantation. TEM caused minimal, transient GVHD whereas central memory T cells (TCM) caused potent GVHD. Surprisingly, TEM were not inert: they, engrafted, homed to target tissues, and proliferated extensively, but they produced less IFN-γ and their expansion in target tissues was limited at later time points, and local proliferation was reduced. Thus, cell-intrinsic properties independent of repertoire explain the impairment of TEM, which can initiate but cannot sustain expansion and tissue damage.

scholarly journals Differentiation of Antigen-Specific T Cells with Limited Functional Capacity during Mycobacterium tuberculosis Infection

2013 ◽  
Vol 82 (1) ◽  
pp. 132-139 ◽  
Author(s):  
Yun Hee Jeong ◽  
Bo-Young Jeon ◽  
Sun-Hwa Gu ◽  
Sang-Nae Cho ◽  
Sung Jae Shin ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Memory T Cells ◽  
Interleukin 2 ◽  
Effector Memory ◽  
Memory Cells ◽  
Content Type ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACTDespite the generation ofMycobacterium tuberculosis-specific T cell immune responses during the course of infection, only 5 to 10% of exposed individuals develop active disease, while others develop a latent infection. This phenomenon suggests defectiveM. tuberculosis-specific immunity, which necessitates more careful characterization ofM. tuberculosis-specific T cell responses. Here, we longitudinally analyzed the phenotypes and functions ofM. tuberculosis-specific T cells. In contrast to the functional exhaustion of T cells observed after chronic infection,M. tuberculosis-specific CD8+T cells differentiated into either effector (CD127loCD62Llo) or effector memory (CD127hiCD62Llo) cells, but not central memory cells (CD127hiCD62Lhi), with low programmed death 1 (PD-1) expression, even in the presence of high levels of bacteria. Additionally,M. tuberculosis-specific CD8+and CD4+T cells produced substantial levels of tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ), but not interleukin 2 (IL-2), uponin vitrorestimulation. AmongM. tuberculosis-specific CD8+T cells, CD127hieffector memory cells displayed slower ongoing turnover but greater survival potential. In addition, these cells produced more IFN-γ and TNF-α and displayed lytic activity upon antigen stimulation. However, the effector function ofM. tuberculosis-specific CD8+CD127hieffector memory T cells was inferior to that of canonical CD8+CD127himemory T cells generated after acute lymphocytic choriomeningitis virus infection. Collectively, our data demonstrate thatM. tuberculosis-specific T cells can differentiate into memory T cells during the course ofM. tuberculosisinfection independent of the bacterial burden but with limited functionality. These results provide a framework for further understanding the mechanisms ofM. tuberculosisinfection that can be used to develop more effective vaccines.

scholarly journals CC Chemokine Receptor 7 Expression by Effector/Memory CD4+ T Cells Depends on Antigen Specificity and Tissue Localization during Influenza A Virus Infection

2004 ◽  
Vol 78 (14) ◽  
pp. 7528-7535 ◽  
Author(s):  
Gudrun F. Debes ◽  
Kerstin Bonhagen ◽  
Thorsten Wolff ◽  
Ute Kretschmer ◽  
Stefan Krautwald ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Memory T Cells ◽  
Effector Memory ◽  
Effector Memory T Cells ◽  
Ifn Γ ◽  
Influenza A Virus Infection ◽  
Cc Chemokine Receptor 7

ABSTRACT The lung is an important entry site for respiratory pathogens such as influenza A virus. In order to combat such invading infectious agents, effector/memory T cells home to the lung and other peripheral tissues as well as lymphoid organs. In this process, chemokines and their receptors fulfill important roles in the guidance of T cells into such organs and specialized microenvironments within tissues. In this study, we determined if CD4+ T cells residing in different lung compartments and draining lymph nodes of influenza A virus-infected and naïve mice express receptors allowing their recirculation into secondary lymphoid tissues. We found high levels of l-selectin and CC chemokine receptor 7 (CCR7) expression in lung-derived CD4+ T cells, similar to that detected on T cells in secondary lymphoid organs. Upon influenza A virus infection, the bulk of gamma interferon-positive (IFN-γ+) and IFN-γ− CD4+ T cells recovered from lung parenchyma retained functional CCR7, whereas virus-specific IFN-γ-producing T cells were CCR7−. In contrast, a majority of virus-specific IFN-γ+ T cells in the lung draining lymph node were CCR7+. Independent of infection, CD4+ T cells obtained from the lung airways exhibited the lowest expression level of l-selectin and CCR7, indicating that T cells at this anatomical site represent the most differentiated effector cell type, lacking the ability to recirculate. Our results suggest that effector/memory T cells that enter inflammatory sites retain functional CCR7 expression, which is lost only upon response to viral antigen and after localization to the final effector site.

Human CMVpp65-Specific Stem Cell-like Memory T-Cells (TSCM) Are a Principal Source for Rapid Repopulation of Immunodominant Central Memory (TCM) and Effector Memory (TEM) in the Circulation

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5728-5728
Author(s):  
Tzu-Yun Kuo ◽  
Aisha Hasan ◽  
Manuel Guerreiro ◽  
Richard J. O'Reilly
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Amino Acid Sequences ◽  
T Cell Subsets ◽  
Effector Memory ◽  
Tnf Α ◽  
Artificial Antigen ◽  
Ifn Γ ◽  
Antigen Presenting

Abstract Latent CMV infection is controlled by a limited repertoire of immunodominant T-cells specific for viral peptides, particularly CMVpp65 and CMV IE-1. The antigen-specific T-cell subsets responsible for maintaining memory T-cells in this repertoire and repopulating them in response to periodic viral reactivations remain unclear. In this study, we generated T-cells specific for CMVpp65 from naïve (TN), TSCM, TCM and TEM subsets isolated from the blood of HLA-A*0201 normal seropositive donors and then comparatively characterized NLV-HLA-A*0201 Tetramer+ T-cells from each of these subsets. Following in vitro sensitization with artificial antigen-presenting cells transduced to express HLA-A*0201 and CMVpp65 and expansion with IL-7, IL-15 and IL-2, Tet+ T-cells were regularly generated from CD62L+CD45RO-CD95- TN and from CD62L+CD45RO-CD95+ TSCM, as well as TCM and TEM. Isolated Tet+ TN, TSCM, TCM and TEM were each able to generate IFN-γ, TNF-α and granzyme B. Each Tet+ subset also expressed similar level of PD-1 and KLRG-1. However, Tet+ TN and TSCM expressed higher levels of CD27 and lower levels of CD57 than TCM or TEM. Tet+ TSCM were distinguished from Tet+ TN, TCM and TEM by a significantly greater level of proliferation and by their rapid and selective expansion of NLV-specific T-cells bearing TCRs identical by amino acid sequences to those expressed by TEM and TCM in the blood. Thus, Tet+ TSCM rather than Tet+ TN constitute the principal repertoire for repopulation of immunodominant memory T-cells sustained in the circulation. Disclosures Hasan: Atara: Patents & Royalties.

scholarly journals Human Fetal TNF-α-Cytokine-Producing CD4+ Effector Memory T Cells Promote Intestinal Development and Mediate Inflammation Early in Life

Immunity ◽  
2019 ◽  
Vol 50 (2) ◽  
pp. 462-476.e8 ◽  
Author(s):  
Renée R.C.E. Schreurs ◽  
Martin E. Baumdick ◽  
Adrian F. Sagebiel ◽  
Max Kaufmann ◽  
Michal Mokry ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Effector Memory ◽  
Intestinal Development ◽  
Effector Memory T Cells ◽  
Tnf Α ◽  
Mediate Inflammation
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