Fc receptor and integrin signaling in phagocytes

Rosales, Carlos

doi:10.1002/sita.200700141

Cited by 27 publications

(42 citation statements)

References 140 publications

(171 reference statements)

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“…Then, the membrane surrounds the target particle and within few minutes it closes at the distal end, leaving a new phagosome. The signaling cascades are known in great detail for the Fc receptors and the complement receptors, since these are the best-studied phagocytic receptors [38, 67, 68]. Signaling for other phagocytic receptors is just beginning to be explored.…”

Section: Particle Internalizationmentioning

confidence: 99%

Phagocytosis: A Fundamental Process in Immunity

Rosales

Uribe‐Querol

2017

BioMed Research International

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One hundred years have passed since the death of Élie Metchnikoff (1845–1916). He was the first to observe the uptake of particles by cells and realized the importance of this process for the host response to injury and infection. He also was a strong advocate of the role of phagocytosis in cellular immunity, and with this he gave us the basis for our modern understanding of inflammation and the innate and acquired immune responses. Phagocytosis is an elegant but complex process for the ingestion and elimination of pathogens, but it is also important for the elimination of apoptotic cells and hence fundamental for tissue homeostasis. Phagocytosis can be divided into four main steps: (i) recognition of the target particle, (ii) signaling to activate the internalization machinery, (iii) phagosome formation, and (iv) phagolysosome maturation. In recent years, the use of new tools of molecular biology and microscopy has provided new insights into the cellular mechanisms of phagocytosis. In this review, we present a general view of our current knowledge on phagocytosis. We emphasize novel molecular findings, particularly on phagosome formation and maturation, and discuss aspects that remain incompletely understood.

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Section: Particle Internalizationmentioning

confidence: 99%

Phagocytosis: A Fundamental Process in Immunity

Rosales

Uribe‐Querol

2017

BioMed Research International

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407

312

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“…1C). Taken together, these results suggested that Fc␥RIIIB leads to Elk-1 activation in the nucleus via a signaling pathway that is independent of most molecules reported to participate in Fc␥R signaling (31).…”

Section: Fc␥riiib Induces Nuclear Factor Elk-1 Activation In Neutrophilsmentioning

confidence: 59%

“…Fc␥RIIA contains a cytoplasmic tail with a well-defined ITAM sequence (43). Upon cross-linking, this receptor initiates a signaling pathway that involves activation of Syk, PI3K, and also ERK (31). All of these molecules are also important for phagocytosis (22).…”

Section: Discussionmentioning

confidence: 99%

FcγRIIA and FcγRIIIB Mediate Nuclear Factor Activation through Separate Signaling Pathways in Human Neutrophils

García‐García

Nieto-Castañeda

Ruiz-Saldaña

et al. 2009

The Journal of Immunology

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Receptors for IgG Abs (Fcγ receptors) are capable of triggering diverse cell responses in leukocytes. In neutrophils, two Fcγ receptors, namely FcγRIIA and FcγRIIIB, are constitutively expressed. The signaling pathways that regulate FcγRIIA-mediated phagocytosis have been relatively well described. However, the different signaling pathways that lead to NF activation after engagement of each Fcγ receptor have only been partially described. To address this problem, neutrophils were stimulated by cross-linking selectively each type of Fcγ receptor with specific mAbs, and NF activation was then analyzed. FcγRIIIB, but not FcγRIIA, promoted a robust increase in phosphorylated ERK in the nucleus, and also efficient phosphorylation of the NF Elk-1. Complete mAb 3G8 (anti-FcγRIIIB) induced a higher response than did F(ab′)2 fragments of mAb 3G8, suggesting a possible synergistic effect of both FcγR receptors. However, mAb IV.3 (anti-FcγRIIA) alone did not cause an increase of phosphorylated ERK in the nucleus. FcγRIIIB-induced nuclear phosphorylation of ERK, and of Elk-1, was not affected by Syk, PI3K, or MEK inhibitors. In contrast, FcγRIIA- or FcγRIIIB-mediated phosphorylation of cytoplasmic ERK depended on Syk, PI3K, and MEK. Also, ERK, but not MEK, was constitutively present in the nucleus, and FcγRIIIB cross-linking did not increase the levels of nuclear ERK or MEK. These data clearly show that different neutrophil Fcγ receptors possess different signaling capabilities. FcγRIIIB, but not FcγRIIA, activates a unique signaling pathway leading to the nuclear-restricted phosphorylation of ERK and Elk-1, independently of Syk, PI3K, or MEK.

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“…FcγRIIIB, but not FcγRIIA, promoted a robust increase in phosphorylated ERK in the nucleus, and also efficient phosphorylation of the nuclear factor Elk-1 [79]. Interestingly, the FcγRIIA signaling pathway resembles the classical ITAM-mediated pathway (Figure 2) [5], while FcγRIIIB signaling pathway remains a mystery (Figure 8). Taken together, these reports strongly support the hypothesis that each FcγR is capable of initiating particular signaling pathways that lead to unique cell responses.…”

Section: Each Fcγr Initiates Particular Signaling Pathways That Lead mentioning

confidence: 98%

“…These antibodies present low affinity for microbial antigens, but they can easily activate the classical complement pathway. Complement deposited on microorganisms can induce phagocytosis via complement receptors [5,6], or it can induce bacterial lysis via the formation of the membrane attack complex [7]. At later times of the adaptive response, antibodies belong mainly to the IgG class.…”

Section: Introductionmentioning

confidence: 99%

Fc receptors: Cell activators of antibody functions

Rosales¹,

Uribe‐Querol²

2013

ABB

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At the onset of an infection early defense systems, such as complement, get into action. Specialized leukocytes (white blood cells) of the innate immune system, including monocytes, macrophages, and neutrophils also participate as a first line of defense against infections. These early responses are rapid but not very specific and are usually not enough to clear completely many infections. The adaptive immune system is also needed to finish the job against many microorganisms. Antibody molecules, produced during the adaptive immune response, are crucial for preventing recurrent infections. Although, IgG antibodies are essential for controlling infections, these molecules do not directly damage the microorganisms they recognize. Today, it is established that leukocytes of the innate immune system are responsible for the protective effects of these antibodies. IgG molecules bind to their cognate antigens and are in turn recognized by specific receptors (Fcγ receptors) on the membrane of leukocytes. Crosslinking these receptors on the surface of leukocytes leads to activation of several effector cell functions. These effector functions are geared toward the destruction of microbial pathogens and the induction of an inflammatory state that is beneficial during infections. However, in autoimmune diseases, antibodies can direct these effector functions against normal tissues and cause severe tissue damage. In recent years, several factors that can modulate the IgG-FcγR interaction have been elucidated. In this review, we describe the main types of Fcγ receptors, and our current view of how antibody variants interact with these receptors to initiate different cell responses. In addition, new findings on the signaling role of individual Fcγ receptors are also discussed.

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Fc receptor and integrin signaling in phagocytes

Cited by 27 publications

References 140 publications

Phagocytosis: A Fundamental Process in Immunity

Phagocytosis: A Fundamental Process in Immunity

FcγRIIA and FcγRIIIB Mediate Nuclear Factor Activation through Separate Signaling Pathways in Human Neutrophils

Fc receptors: Cell activators of antibody functions

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