Increase in neutrophil Fc gamma receptor I expression following interferon gamma treatment in rheumatoid arthritis.

Goulding, N. J.; Knight, Scott; Godolphin, J L; Guyre, Paul M.

doi:10.1136/ard.51.4.465

Cited by 25 publications

(11 citation statements)

References 16 publications

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“…Whereas FcγR expression is rather well-described qualitatively, there is only quite limited information available on actual numbers of FcγR expressed by the different leukocyte populations (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). To our knowledge there is no publication, where such numbers have been determined for the main leukocyte populations in parallel, even though Antal-Szalmas et al (18) and the group of Guyre (19,(22)(23)(24)(25) provided data on human neutrophils and monocytes. In addition, work on FcγR cell surface numbers often dates back to times, where certain cell subpopulations with an entirely different FcγR repertoire (such as classical and non-classical monocytes), had not been distinguished.…”

Section: Introductionmentioning

confidence: 99%

There Is (Scientific) Strength in Numbers: A Comprehensive Quantitation of Fc Gamma Receptor Numbers on Human and Murine Peripheral Blood Leukocytes

2020

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Antibodies are essential mediators of immunological defense mechanisms, are clinically used as therapeutic agents, but are also functionally involved in various immune-mediated disorders. Whereas IgG antibodies accomplish some of their biological tasks autonomously, many functions depend on their binding to activating and inhibitory Fcγ receptors (FcγR). From a qualitative point of view expression patterns of FcγR on immunologically relevant cell types are well-characterized both for mice and humans. Surprisingly, however, there is only quite limited information available on actual quantities of FcγR expressed by the different leukocyte populations. In this study we provide a comprehensive data set assessing quantitatively how many individual human and mouse FcγRs are expressed on B cells, NK cells, eosinophils, neutrophils, basophils and both classical, and non-classical monocytes under steady state conditions. Moreover, among human donors we found two groups with different expression levels of the inhibitory FcγRIIb on monocytes which appears to correlate with haplotypes of the activating FcγRIIIa.

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Section: Introductionmentioning

confidence: 99%

There Is (Scientific) Strength in Numbers: A Comprehensive Quantitation of Fc Gamma Receptor Numbers on Human and Murine Peripheral Blood Leukocytes

2020

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“…The patients are described under subjects, group 4. represents an effect of granulocyte colony-stimulating factor (G-CSF), the concentration of which is markedly elevated in cord blood from most term and preterm neonates [9]. In addition to G-CSF, interferon-g (IFN-g) is the only cytokine known to induce the expression of CD64 on neutrophils [10][11][12][13]. Both these cytokines are produced in response to bacterial infections.…”

Section: Discussionmentioning

confidence: 99%

CD64 (Fcγ receptor I) cell surface expression on maturing neutrophils from preterm and term newborn infants

Fjaertoft¹,

Håkansson

Foucard³

et al. 2005

Acta Paediatrica

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“…In vitro experiments also showed that expression of FcγRIIIa is up-regulated by TGF-β, IFN-γ and M-CSF [138]; expression of FcγRI is up-regulated by G-CSF and IFN-γ [139–141]. Also, rheumatoid arthritis patients treated with IFN-γ have increase in neutrophil FcγRI expression [142]. Dysregulation and dysfunction of FcγRs are often observed at sites of inflammation in autoimmune diseases.…”

Section: Future Strategiesmentioning

confidence: 99%

Targeting the Fc receptor in autoimmune disease

Kimberly

2014

Expert Opinion on Therapeutic Targets

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Introduction The Fc receptors and their interaction with immunoglobulin and innate immune opsonins such as CRP are key players in humoral and cellular immune responses. As the effector mechanism for some therapeutic monoclonal antibodies and often a contributor to the pathogenesis and progression of autoimmunity, FcRs are promising targets for treating autoimmune diseases. Areas covered This review discusses the nature of different Fc receptors and the various mechanisms of their involvement in initiating and modulating immunocyte functions and their biological consequences. It describes a range of current strategies in targeting Fc receptors and manipulating their interaction with specific ligands while presenting the pros and cons of these approaches. This review also discusses potential new strategies including regulation of FcR expression and receptor cross-talk. Expert opinion Fc receptors are appealing targets in the treatment of inflammatory autoimmune diseases. However, there are still knowledge limitations and technical challenges, the most important being a better understanding of the individual roles of each of the Fc receptors and enhancement of the specificity in targeting particular cell types and specific Fc receptors.

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Increase in neutrophil Fc gamma receptor I expression following interferon gamma treatment in rheumatoid arthritis.

Cited by 25 publications

References 16 publications

There Is (Scientific) Strength in Numbers: A Comprehensive Quantitation of Fc Gamma Receptor Numbers on Human and Murine Peripheral Blood Leukocytes

There Is (Scientific) Strength in Numbers: A Comprehensive Quantitation of Fc Gamma Receptor Numbers on Human and Murine Peripheral Blood Leukocytes

CD64 (Fcγ receptor I) cell surface expression on maturing neutrophils from preterm and term newborn infants

Targeting the Fc receptor in autoimmune disease

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