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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 in autoimmune disease with rheumatoid arthritis as an example.Immunocomplexes activate neutrophils, which in turn release proteases damagingthe cartilage. Induction of oxidative bursts generates reactive oxygen species(ROS), which also directly damage the articular cartilage. In addition, B-cellactivating factor (BAFF) secretion activates B cells. Receptor activator ofnuclear factor kappa-B ligand (RANKL) production by neutrophils has been shownin mature peripheral neutrophils. In bone, preliminary data indicate that RANKLderived from neutrophils in the bone marrow might participate in bonemetabolism.
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f03: Neutrophils in autoimmune disease with rheumatoid arthritis as an example.Immunocomplexes activate neutrophils, which in turn release proteases damagingthe cartilage. Induction of oxidative bursts generates reactive oxygen species(ROS), which also directly damage the articular cartilage. In addition, B-cellactivating factor (BAFF) secretion activates B cells. Receptor activator ofnuclear factor kappa-B ligand (RANKL) production by neutrophils has been shownin mature peripheral neutrophils. In bone, preliminary data indicate that RANKLderived from neutrophils in the bone marrow might participate in bonemetabolism.

Mentions: RA is a systemic inflammatory disorder that primarily affects the joints, causingpain and loss of function. Neutrophils from the blood of RA patients are primed tosecrete high levels of ROS and cytokines (43).Activation of neutrophils through recognition of immune complexes by FcγRs inducesdegranulation with an increase in granule proteins in the synovia, leading tocartilage damage. ROS production is also augmented, which increases NET release andexposes granule contents and cytoplasmic and citrullinated autoantigens in the joints(44). These neutrophils can also secretehigh levels of receptor activator of nuclear factor kappa-B ligand (RANKL) (45) and BAFF (46), which activate osteoclasts and B cells, respectively (Figure 3). In addition, neutrophils from RApatients upregulate MHC-II expression and increase the antigen presentation abilityof neutrophils, leading to T-cell activation (47). The contribution of neutrophils to RA pathology can be seen inFelty’s syndrome (a severe form of RA) where the diagnostic findings includesplenomegaly, high neutrophil counts, and autoantibodies against PAD-4, an argininedeaminase that converts arginine to citrulline that bind to neutrophils and NETs(48).


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 in autoimmune disease with rheumatoid arthritis as an example.Immunocomplexes activate neutrophils, which in turn release proteases damagingthe cartilage. Induction of oxidative bursts generates reactive oxygen species(ROS), which also directly damage the articular cartilage. In addition, B-cellactivating factor (BAFF) secretion activates B cells. Receptor activator ofnuclear factor kappa-B ligand (RANKL) production by neutrophils has been shownin mature peripheral neutrophils. In bone, preliminary data indicate that RANKLderived from neutrophils in the bone marrow might participate in bonemetabolism.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f03: Neutrophils in autoimmune disease with rheumatoid arthritis as an example.Immunocomplexes activate neutrophils, which in turn release proteases damagingthe cartilage. Induction of oxidative bursts generates reactive oxygen species(ROS), which also directly damage the articular cartilage. In addition, B-cellactivating factor (BAFF) secretion activates B cells. Receptor activator ofnuclear factor kappa-B ligand (RANKL) production by neutrophils has been shownin mature peripheral neutrophils. In bone, preliminary data indicate that RANKLderived from neutrophils in the bone marrow might participate in bonemetabolism.
Mentions: RA is a systemic inflammatory disorder that primarily affects the joints, causingpain and loss of function. Neutrophils from the blood of RA patients are primed tosecrete high levels of ROS and cytokines (43).Activation of neutrophils through recognition of immune complexes by FcγRs inducesdegranulation with an increase in granule proteins in the synovia, leading tocartilage damage. ROS production is also augmented, which increases NET release andexposes granule contents and cytoplasmic and citrullinated autoantigens in the joints(44). These neutrophils can also secretehigh levels of receptor activator of nuclear factor kappa-B ligand (RANKL) (45) and BAFF (46), which activate osteoclasts and B cells, respectively (Figure 3). In addition, neutrophils from RApatients upregulate MHC-II expression and increase the antigen presentation abilityof neutrophils, leading to T-cell activation (47). The contribution of neutrophils to RA pathology can be seen inFelty’s syndrome (a severe form of RA) where the diagnostic findings includesplenomegaly, high neutrophil counts, and autoantibodies against PAD-4, an argininedeaminase that converts arginine to citrulline that bind to neutrophils and NETs(48).

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