Cutting Edge: Local Recall Responses by Memory T Cells Newly Recruited to Peripheral Nonlymphoid Tissues

Wakim, Linda M.; Gebhardt, Thomas; Heath, William R.; Carbone, Francis R.

doi:10.4049/jimmunol.181.9.5837

Cited by 61 publications

(51 citation statements)

References 23 publications

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“…same way, memory T cells are nonspecifically recruited early to sites of infection (84). It is possible, though, that within this population of early T cell recruits exists a population of activated effector memory cells capable of cross-reacting with ANDV epitopes or activated naïve T cells (such as T h 2 cells) that have not undergone proliferation (3,11,43) but that may initiate a pathway to disease pathogenesis before being depleted.…”

Section: Vol 85 2011 T Cells Are Not Required For Hps Pathogenesis mentioning

confidence: 99%

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

Hammerbeck

Hooper

2011

J Virol

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Andes virus (ANDV) is associated with a lethal vascular leak syndrome in humans termed hantavirus pulmonary syndrome (HPS). In hamsters, ANDV causes a respiratory distress syndrome closely resembling human HPS. The mechanism for the massive vascular leakage associated with HPS is poorly understood; however, T cell immunopathology has been implicated on the basis of circumstantial and corollary evidence. Here, we show that following ANDV challenge, hamster T cell activation corresponds with the onset of disease. However, treatment with cyclophosphamide or specific T cell depletion does not impact the course of disease or alter the number of surviving animals, despite significant reductions in T cell number. These data demonstrate, for the first time, that T cells are not required for hantavirus pathogenesis in the hamster model of human HPS. Depletion of T cells from Syrian hamsters did not significantly influence early events in disease progression. Moreover, these data argue for a mechanism of hantavirus-induced vascular permeability that does not involve T cell immunopathology.

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Section: Vol 85 2011 T Cells Are Not Required For Hps Pathogenesis mentioning

confidence: 99%

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

Hammerbeck

Hooper

2011

J Virol

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“…The present data and other recent data suggest that the contribution of further activation signals in the target tissue has been understated. 11,31,32 Once in the islet environment, CTLs increased their cytotoxic effector capacity. This increase requires location-specific signals that are independent of the ␤ cell.…”

Section: Discussionmentioning

confidence: 99%

Autoreactive Cytotoxic T Lymphocytes Acquire Higher Expression of Cytotoxic Effector Markers in the Islets of NOD Mice after Priming in Pancreatic Lymph Nodes

Graham

Krishnamurthy

Fynch

et al. 2011

The American Journal of Pathology

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Cytotoxic T lymphocytes (CTLs) that cause type 1 diabetes are activated in draining lymph nodes and become concentrated as fully active CTLs in inflamed pancreatic islets. It is unclear whether CTL function is driven by signals received in the lymph node or also in the inflamed tissue. We studied whether the development of cytotoxicity requires further activation in islets. Autoreactive CTLs found in the islets of diabetes-prone NOD mice had acquired much higher expression of the cytotoxic effector markers granzyme B, interferon ␥, and CD107a than had those in the pancreatic lymph node (PLN). Increased expression seemed to result from stimulation in the islet itself. T cells held up from migrating from the PLN by administration of the sphingosine-1-phosphate agonist FTY720 did not increase expression of cytotoxic molecules in the PLN. Stimulation did not require antigen presentation or cytokine secretion by the target ␤ cells because it was not affected by the absence of class I major histocompatibility complex expression or by the overexpression of suppressor of cytokine signaling-1. Activation of CD40-expressing cells stimulated increased CTL function and ␤-cell destruction, suggesting that signals derived from CD40-expressing cells promote the acquisition of cytotoxicity in the islet environment. These data provide in vivo evidence that stimulation of cytotoxic effector molecule expression occurs in inflamed islets and is independent of ␤ cells.

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“…1B). These cells might play a role in the additional activation of LN-primed T cells and/or be important as local antigen-presenting cells that stimulate effector/memory T cells that are directly recruited to inflammatory sites (37,48,49). Furthermore, they could also play a role in the production of cytokines and chemokines that are involved in the attraction of different inflammatory cell types (13).…”

Section: Discussionmentioning

confidence: 99%

Respiratory Syncytial Virus-Induced Activation and Migration of Respiratory Dendritic Cells and Subsequent Antigen Presentation in the Lung-Draining Lymph Node

Lukens

Kruijsen

Coenjaerts

et al. 2009

J Virol

109

113

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In the respiratory tract, different dendritic cell (DC) populations guard a tight balance between tolerance and immunity to infectious or harmless materials to which the airways are continuously exposed. For infectious and noninfectious antigens administered via different routes, different subsets of DC might contribute during the induction of T-cell tolerance and immunity. We studied the impact of primary respiratory syncytial virus (RSV) infection on respiratory DC composition in C57BL/6 mice. We also tracked the migration of respiratory DC to the lymph nodes and studied antigen presentation by lung-derived and lymph node-resident DC to CD4

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Cutting Edge: Local Recall Responses by Memory T Cells Newly Recruited to Peripheral Nonlymphoid Tissues

Cited by 61 publications

References 23 publications

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

Autoreactive Cytotoxic T Lymphocytes Acquire Higher Expression of Cytotoxic Effector Markers in the Islets of NOD Mice after Priming in Pancreatic Lymph Nodes

Respiratory Syncytial Virus-Induced Activation and Migration of Respiratory Dendritic Cells and Subsequent Antigen Presentation in the Lung-Draining Lymph Node

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