Cytokine release from innate immune cells: association with diverse membrane trafficking pathways

Lacy, Paige; Stow, Jennifer L.

doi:10.1182/blood-2010-08-265892

Cited by 325 publications

(281 citation statements)

References 104 publications

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“…We also show that Rab27a and hMunc13-4 endosomal exocytic vesicles are likely distinct from CCL5V, and that both types of granules strongly colocalize and potentially fuse at the IS in a manner similar to that with CG. Moreover, our results indicate that Rab27a and hMunc13-4 deficiencies lead to multifocal secretion of CCL5, most likely in a piecemeal manner by shuttling the chemokine, through a pool of smaller secretory vesicles, from CCL5V throughout the T cell surface (37,38). These data suggest that CCL5V and CG use the same Rab27a-hMunc13-4-dependent mechanism for their synaptic release, resulting in a high local concentration of the chemokine, concomitant with target cell killing.…”

Section: Discussionmentioning

confidence: 64%

Synaptic Release of CCL5 Storage Vesicles Triggers CXCR4 Surface Expression Promoting CTL Migration in Response to CXCL12

Franciszkiewicz

Boutet

Gauthier

et al. 2014

The Journal of Immunology

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The lytic function of CTL relies on the polarized release of cytotoxic granules (CG) at the immune synapse (IS) with target cells. CTL also contain CCL5 in cytoplasmic storage vesicles (CCL5V) distinct from CG, the role of which, in regulating T cell effector functions, is not understood. Using human CD8+ T cells specific to a lung tumor–associated Ag, we show in this article that CTL release both secretory compartments into the immune synapse with autologous tumor cells. Moreover, we demonstrate that disorganization of the T cell microtubule cytoskeleton and defects in hMunc13-4 or Rab27a abrogate CG exocytosis and synaptic secretion of the chemokine. Mechanistically, synaptic release of CCL5 cytoplasmic storage vesicles likely occurs upon their coalescence with the Rab27a-hMunc13-4 compartment and results in autocrine, CCR5-dependent induction of CXCR4 cell surface expression, thereby promoting T cell migration in response to CXCL12. We propose that CCL5 polarized delivery represents a mechanism by which CTL control immune synapse duration.

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Section: Discussionmentioning

confidence: 64%

Synaptic Release of CCL5 Storage Vesicles Triggers CXCR4 Surface Expression Promoting CTL Migration in Response to CXCL12

Franciszkiewicz

Boutet

Gauthier

et al. 2014

The Journal of Immunology

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“…In time, constant viral replication and immune activation cause further decrease in CD4+ T-cell counts, immune system loses control over infection leading to opportunistic infections, malignancies and death of untreated individuals [3]. Cytokines are biological response modifiers synthesized by cells of innate and adaptive immunity that are important in intercellular communication and regulation of immune reactions [9], [10], [11] and [12]. Effector functions of CD4+ T-cells depend on cytokine immunity.…”

Section: Introductionmentioning

confidence: 99%

The comparison of Th1, Th2, Th9, Th17 and Th22 cytokine profiles in acute and chronic HIV-1 infection

Gorenec

Lepej

Grgic

et al. 2016

Microbial Pathogenesis

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“…PMN and Mf synthesize multiple cytokines and chemokines, including TNF-a (24,45,46). As well, we and others have shown that some components of the complement cascade, specifically C1q and C3, are synthesized by PMN and Mf both in vitro and in vivo following neurodegeneration (47)(48)(49).…”

Section: Pmn-and Mf-cm Factorsmentioning

confidence: 99%

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Hooshmand

Nguyen

Piltti

et al. 2017

The Journal of Immunology

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Inflammatory processes play a key role in pathophysiology of many neurologic diseases/trauma, but the effect of immune cells and factors on neurotransplantation strategies remains unclear. We hypothesized that cellular and humoral components of innate immunity alter fate and migration of human neural stem cells (hNSC). In these experiments, conditioned media collected from polymorphonuclear leukocytes (PMN) selectively increased hNSC astrogliogenesis and promoted cell migration in vitro. PMN were shown to generate C1q and C3a; exposure of hNSC to PMN-synthesized concentrations of these complement proteins promoted astrogliogenesis and cell migration. Furthermore, in vitro, Abs directed against C1q and C3a reversed the fate and migration effects observed. In a proof-of-concept in vivo experiment, blockade of C1q and C3a transiently altered hNSC migration and reversed astroglial fate after spinal cord injury. Collectively, these data suggest that modulation of the innate/humoral inflammatory microenvironment may impact the potential of cell-based therapies for recovery and repair following CNS pathology.

show abstract

Cytokine release from innate immune cells: association with diverse membrane trafficking pathways

Cited by 325 publications

References 104 publications

Synaptic Release of CCL5 Storage Vesicles Triggers CXCR4 Surface Expression Promoting CTL Migration in Response to CXCL12

Synaptic Release of CCL5 Storage Vesicles Triggers CXCR4 Surface Expression Promoting CTL Migration in Response to CXCL12

The comparison of Th1, Th2, Th9, Th17 and Th22 cytokine profiles in acute and chronic HIV-1 infection

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

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