The Leukotriene B4 Receptor (BLT1) Is Required for Effector CD8+ T Cell-Mediated, Mast Cell-Dependent Airway Hyperresponsiveness

Taube, Christian; Miyahara, Nobuaki; Ott, Vanessa; Swanson, Brad; Takeda, Katsuyuki; Loader, Joan E.; Shultz, Leonard D.; Tager, Andrew M.; Luster, Andrew D.; Dakhama, Azzeddine; Gelfand, Erwin W.

doi:10.4049/jimmunol.176.5.3157

Cited by 96 publications

(92 citation statements)

References 55 publications

(61 reference statements)

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“…Considering the major role of LTB 4 and cys-LTs in mast cell biology and infl ammatory regulation ( 6,7,10 ), the phenotype-specifi c differences in concentration and relative abundance of LTC 4 versus LTB 4 will most likely have biological implications. For example, numerous studies have established the impact of LTs in recruitment of T-cells and dendritic cells and in development of allergic airway disease ( 11,12,50 ). Data also indicate that LTC 4 and LTD 4 are key players in fi brosis and vascular injury via the CysLT2 receptor, and they have been implicated in the pathogenesis of human abdominal aortic aneurysm ( 17,18,51 ).…”

Section: Integrated Multivariate Modelingmentioning

confidence: 99%

Lipid mediator metabolic profiling demonstrates differences in eicosanoid patterns in two phenotypically distinct mast cell populations

Lundström¹,

Saluja

Adner

et al. 2013

Journal of Lipid Research

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Mast cells are important multifunctional infl ammatory cells that are particularly well known for their involvement in allergic diseases; however, they are also implicated in many physiological and pathophysiological functions in health and disease ( 1 ). Mast cells are distributed in all tissues and are particularly numerous in those tissues that are in close contact with the environment, e.g., the skin, the gastrointestinal tract, and the respiratory system ( 2 ). They express a variety of receptors that recognize both endogenous (e.g., cytokines, neuropeptides, complement) and exogenous molecules (e.g., pathogen-derived molecules, allergens through IgE receptor cross-linking). Upon recognition and activation, the cells have the capacity to

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Section: Integrated Multivariate Modelingmentioning

confidence: 99%

Lipid mediator metabolic profiling demonstrates differences in eicosanoid patterns in two phenotypically distinct mast cell populations

Lundström¹,

Saluja

Adner

et al. 2013

Journal of Lipid Research

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“…Mast cells in the periphery enhance effector T cell recruitment directly by the production of chemoattractants. LTB 4 from mast cells recruits CD8 cells, 104 and IL-16 recruits CD4 cells. 46 Mast cells also recruit effector T cells indirectly by their cytokine activation of local vascular endothelia enhancing the expression of intercellular adhesion molecule 1 and vascular cellular adhesion molecule, leukocyte adherence, and transmigration.…”

Section: Role Of Mast Cells In Inflammatory and Autoimmune Kidney Dismentioning

confidence: 99%

Role of Mast Cells in Progressive Renal Diseases

Holdsworth¹,

Summers²

2008

Journal of the American Society of Nephrology

116

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“…Recently, effector memory CD8 ϩ T cells but not central memory CD8 ϩ T cells were shown to be essential for the development of AHR and airway allergic inflammation in adoptive transfer models (28,29).…”

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confidence: 99%

CD8+ T Cell-Mediated Airway Hyperresponsiveness and Inflammation Is Dependent on CD4+IL-4+ T Cells

Koya

Miyahara

Takeda

et al. 2007

The Journal of Immunology

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CD4+ T cells, particularly Th2 cells, play a pivotal role in allergic airway inflammation. However, the requirements for interactions between CD4+ and CD8+ T cells in airway allergic inflammation have not been delineated. Sensitized and challenged OT-1 mice in which CD8+ T cells expressing the transgene for the OVA257–264 peptide (SIINFEKL) failed to develop airway hyperresponsiveness (AHR), airway eosinophilia, Th2 cytokine elevation, or goblet cell metaplasia. OT-1 mice that received naive CD4+IL-4+ T cells but not CD4+IL-4− T cells before sensitization developed all of these responses to the same degree as wild-type mice. Moreover, recipients of CD4+IL-4+ T cells developed significant increases in the number of CD8+IL-13+ T cells in the lung, whereas sensitized OT-1 mice that received primed CD4+ T cells just before challenge failed to develop these responses. Sensitized CD8-deficient mice that received CD8+ T cells from OT-1 mice that received naive CD4+ T cells before sensitization increased AHR and eosinophil numbers in bronchoalveolar lavage fluid when challenged with allergen. In contrast, sensitized CD8-deficient mice receiving CD8+ T cells from OT-1 mice without CD4+ T cells developed reduced AHR and eosinophil numbers in bronchoalveolar lavage fluid when challenged. These data suggest that interactions between CD4+ and CD8+ T cells, in part through IL-4 during the sensitization phase, are essential to the development of CD8+IL-13+ T cell-dependent AHR and airway allergic inflammation.

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The Leukotriene B4 Receptor (BLT1) Is Required for Effector CD8+ T Cell-Mediated, Mast Cell-Dependent Airway Hyperresponsiveness

Cited by 96 publications

References 55 publications

Lipid mediator metabolic profiling demonstrates differences in eicosanoid patterns in two phenotypically distinct mast cell populations

Lipid mediator metabolic profiling demonstrates differences in eicosanoid patterns in two phenotypically distinct mast cell populations

Role of Mast Cells in Progressive Renal Diseases

CD8+ T Cell-Mediated Airway Hyperresponsiveness and Inflammation Is Dependent on CD4+IL-4+ T Cells

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