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

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.

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 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.

Sign in / Sign up

Export Citation Format

Share Document