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Plasticity of neutrophils reveals modulatory capacity.

Perobelli SM, Galvani RG, Gonçalves-Silva T, Xavier CR, Nóbrega A, Bonomo A - Braz. J. Med. Biol. Res. (2015)

Bottom Line: Neutrophils have also been shown to produce a wide range of cytokines that have pro- or anti-inflammatory activity, adding a modulatory role for this cell, previously known as a suicide effector.The presence of cytokines almost always implies intercellular modulation, potentially unmasking interactions of neutrophils with other immune cells.These cells can switch phenotypes and exert functions beyond cytotoxicity against invading pathogens, extending the view of neutrophils beyond suicide effectors to include functions as regulatory and suppressor cells.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brasil.

ABSTRACT
Neutrophils are widely known as proinflammatory cells associated with tissue damage and for their early arrival at sites of infection, where they exert their phagocytic activity, release their granule contents, and subsequently die. However, this view has been challenged by emerging evidence that neutrophils have other activities and are not so short-lived. Following activation, neutrophil effector functions include production and release of granule contents, reactive oxygen species (ROS), and neutrophil extracellular traps (NETs). Neutrophils have also been shown to produce a wide range of cytokines that have pro- or anti-inflammatory activity, adding a modulatory role for this cell, previously known as a suicide effector. The presence of cytokines almost always implies intercellular modulation, potentially unmasking interactions of neutrophils with other immune cells. In fact, neutrophils have been found to help B cells and to modulate dendritic cell (DC), macrophage, and T-cell activities. In this review, we describe some ways in which neutrophils influence the inflammatory environment in infection, cancer, and autoimmunity, regulating both innate and adaptive immune responses. These cells can switch phenotypes and exert functions beyond cytotoxicity against invading pathogens, extending the view of neutrophils beyond suicide effectors to include functions as regulatory and suppressor cells.

No MeSH data available.


Related in: MedlinePlus

Neutrophils (N) cross-talk with other immune cells and are receptive ofvarious innate or adaptive immunity system stimuli. This figure illustrates anexample of the numerous possibilities for reciprocal regulation. Macrophages (M),along with many other cytokines, produce granulocyte colony-stimulating factor(G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), which canin turn induce production of cytokines such as interleukin (IL)-10 by neutrophils.Under different conditions, neutrophils can modify the extent of majorhistocompatibility complex (MHC) and costimulatory molecule expression, producereactive oxygen species and nitric oxide synthase, or consume arginine leading toinhibition of the T-cell (T) response. TCR: T-cell receptor.
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f02: Neutrophils (N) cross-talk with other immune cells and are receptive ofvarious innate or adaptive immunity system stimuli. This figure illustrates anexample of the numerous possibilities for reciprocal regulation. Macrophages (M),along with many other cytokines, produce granulocyte colony-stimulating factor(G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), which canin turn induce production of cytokines such as interleukin (IL)-10 by neutrophils.Under different conditions, neutrophils can modify the extent of majorhistocompatibility complex (MHC) and costimulatory molecule expression, producereactive oxygen species and nitric oxide synthase, or consume arginine leading toinhibition of the T-cell (T) response. TCR: T-cell receptor.

Mentions: Beyond their individual activity, neutrophils influence effector functions of otherleukocytes in a direct or indirect manner through contact or cytokine production.Neutrophils and macrophages cross-talk through cytokines and chemokines, attracting eachother to inflammatory sites. Also, neutrophils can transfer granule-derived moleculesand ingested materials to macrophages. On the other hand, macrophages produce cytokineslike granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophagecolony-stimulating factor (GM-CSF), which prevent early neutrophil apoptosis. Apoptoticneutrophils and polymorphonuclear (PMN) leukocytes assist macrophages in the resolutionof inflammation but can also activate their companion macrophages, if they are infected,contributing to tissue damage in longer lasting infections. Thus, through a combinationof overlapping and complementary characteristics, the two most important professionalphagocytes contribute to microbial clearance and resolution of inflammation or tissuedamage (Figure 2) (16171819192021).


Plasticity of neutrophils reveals modulatory capacity.

Perobelli SM, Galvani RG, Gonçalves-Silva T, Xavier CR, Nóbrega A, Bonomo A - Braz. J. Med. Biol. Res. (2015)

Neutrophils (N) cross-talk with other immune cells and are receptive ofvarious innate or adaptive immunity system stimuli. This figure illustrates anexample of the numerous possibilities for reciprocal regulation. Macrophages (M),along with many other cytokines, produce granulocyte colony-stimulating factor(G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), which canin turn induce production of cytokines such as interleukin (IL)-10 by neutrophils.Under different conditions, neutrophils can modify the extent of majorhistocompatibility complex (MHC) and costimulatory molecule expression, producereactive oxygen species and nitric oxide synthase, or consume arginine leading toinhibition of the T-cell (T) response. TCR: T-cell receptor.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4541684&req=5

f02: Neutrophils (N) cross-talk with other immune cells and are receptive ofvarious innate or adaptive immunity system stimuli. This figure illustrates anexample of the numerous possibilities for reciprocal regulation. Macrophages (M),along with many other cytokines, produce granulocyte colony-stimulating factor(G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), which canin turn induce production of cytokines such as interleukin (IL)-10 by neutrophils.Under different conditions, neutrophils can modify the extent of majorhistocompatibility complex (MHC) and costimulatory molecule expression, producereactive oxygen species and nitric oxide synthase, or consume arginine leading toinhibition of the T-cell (T) response. TCR: T-cell receptor.
Mentions: Beyond their individual activity, neutrophils influence effector functions of otherleukocytes in a direct or indirect manner through contact or cytokine production.Neutrophils and macrophages cross-talk through cytokines and chemokines, attracting eachother to inflammatory sites. Also, neutrophils can transfer granule-derived moleculesand ingested materials to macrophages. On the other hand, macrophages produce cytokineslike granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophagecolony-stimulating factor (GM-CSF), which prevent early neutrophil apoptosis. Apoptoticneutrophils and polymorphonuclear (PMN) leukocytes assist macrophages in the resolutionof inflammation but can also activate their companion macrophages, if they are infected,contributing to tissue damage in longer lasting infections. Thus, through a combinationof overlapping and complementary characteristics, the two most important professionalphagocytes contribute to microbial clearance and resolution of inflammation or tissuedamage (Figure 2) (16171819192021).

Bottom Line: Neutrophils have also been shown to produce a wide range of cytokines that have pro- or anti-inflammatory activity, adding a modulatory role for this cell, previously known as a suicide effector.The presence of cytokines almost always implies intercellular modulation, potentially unmasking interactions of neutrophils with other immune cells.These cells can switch phenotypes and exert functions beyond cytotoxicity against invading pathogens, extending the view of neutrophils beyond suicide effectors to include functions as regulatory and suppressor cells.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brasil.

ABSTRACT
Neutrophils are widely known as proinflammatory cells associated with tissue damage and for their early arrival at sites of infection, where they exert their phagocytic activity, release their granule contents, and subsequently die. However, this view has been challenged by emerging evidence that neutrophils have other activities and are not so short-lived. Following activation, neutrophil effector functions include production and release of granule contents, reactive oxygen species (ROS), and neutrophil extracellular traps (NETs). Neutrophils have also been shown to produce a wide range of cytokines that have pro- or anti-inflammatory activity, adding a modulatory role for this cell, previously known as a suicide effector. The presence of cytokines almost always implies intercellular modulation, potentially unmasking interactions of neutrophils with other immune cells. In fact, neutrophils have been found to help B cells and to modulate dendritic cell (DC), macrophage, and T-cell activities. In this review, we describe some ways in which neutrophils influence the inflammatory environment in infection, cancer, and autoimmunity, regulating both innate and adaptive immune responses. These cells can switch phenotypes and exert functions beyond cytotoxicity against invading pathogens, extending the view of neutrophils beyond suicide effectors to include functions as regulatory and suppressor cells.

No MeSH data available.


Related in: MedlinePlus