Differential distribution of FcγRIIIa in normal human tissues and co‐localization with DAF and fibrillin‐1: implications for imm_unological microenvironments

Bhatia, Aakanksha; Blades, S.; Cambridge, G; Edwards, Jcw

doi:10.1046/j.1365-2567.1998.00491.x

Cited by 59 publications

(30 citation statements)

References 31 publications

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“…20 In RA, IgG rheumatoid factor (RF) complexes may account for the articular and extra-articular features of RA, 20 ultimately through ligation of Fc␥RIIIa by IgG RF with the subsequent generation of TNF␣, an inflammatory cytokine highly expressed on macrophages in synovium intima and other target tissues. 21,22 Similar mechanisms have been postulated for other autoimmune disorders, such as systemic lupus erythematosus, multiple sclerosis, myasthenia gravis, and progressive systemic sclerosis, 20 which share similar clinical manifestations as chronic GVHD. Immune thrombocytopenia can also be associated with a number of autoimmune disorders.…”

Section: Immunology and Pathology Of Chronic Gvhdmentioning

confidence: 67%

Chronic graft-versus-host disease: clinical manifestation and therapy

Ratanatharathorn

Ayash

Lazarus

et al. 2001

Bone Marrow Transplant

231

149

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Summary:Chronic graft-versus-host disease (GVHD) is a major cause of morbidity and mortality in long-term survivors of allogeneic stem cell transplantation. The immunopathogenesis of chronic GVHD is, in part, TH-2 mediated, resulting in a syndrome of immunodeficiency and an autoimmune disorder. The most important risk factor for chronic GVHD is prior history of acute GVHD and strategies that prevent acute GVHD also decrease the risk of chronic GVHD. Other important risk factors are the use of a non-T cell-depleted graft, and older age of donor and recipient. Whether recipients of peripheral blood stem cells are at increased risk of chronic GVHD remains unsettled. There are no known pharmacologic agents which can specifically prevent development of chronic GVHD. Agents which have efficacy in the treatment of autoimmune disorders have been utilized as therapy for established chronic GVHD and are associated with response rates of 20% to 80%. Most responses are confined to skin, soft tissue, oral mucosa and occasionally liver. Bronchiolitis obliterans responds infrequently to therapy and is associated with a dismal prognosis. Newer, promising therapeutic strategies under investigation include thalidomide, photopheresis therapy, anti-tumor necrosis factor and B cell depletion with anti-CD20 monoclonal antibody. Bone Marrow Transplantation (2001) 28, 121-129.

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Section: Immunology and Pathology Of Chronic Gvhdmentioning

confidence: 67%

Chronic graft-versus-host disease: clinical manifestation and therapy

Ratanatharathorn

Ayash

Lazarus

et al. 2001

Bone Marrow Transplant

231

149

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“…Importantly, CD16 binding is preferential for small IgG dimer or trimer complexes that include IgG-anti-IgG antibody complexes, an important component of rheumatoid factors that are potential triggers for onset or maintenance of RA (23)(24)(25)(26). Furthermore, expression of CD16 on macrophages is restricted to tissues (e.g., synovial tissue, pericardium) impacted by RA, suggesting that the tissue specificity of RA occurs through a mechanism dependent on this receptor (27). Previous studies indicate that Fc␥RI and Fc␥RII have a higher level of expression on splenic macrophages due to estrogen treatment that contributes to clearance of IgG-sensitized cells (28,29).…”

Section: Conclusion Estrogen Can Modulate Proinflammatory Cytokine Rmentioning

confidence: 99%

17β‐estradiol regulates cytokine release through modulation of CD16 expression in monocytes and monocyte‐derived macrophages

Kramer¹,

Krämer²,

Guan³

2004

Arthritis & Rheumatism

174

127

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Objective. Macrophages release cytokines, such as tumor necrosis factor ␣ (TNF␣), interleukin-1 (IL-1), and IL-6, which modulate the symptoms of rheumatoid arthritis (RA). Macrophage release of these cytokines can be modulated by estrogen. Fc␥ receptor type IIIA (CD16a) is a receptor expressed on macrophages that selectively binds IgG molecules, an important rheumatoid factor in RA. Binding of CD16 by anti-CD16 monoclonal antibodies stimulates macrophage cytokine release. We undertook this study to test the hypothesis that decreased concentrations of estrogen (17␤-estradiol) directly cause an increase in CD16 expression, resulting in increased release of proinflammatory cytokines from monocytes and/or macrophages upon receptor binding.Methods. THP-1 cells and female human primary monocytes and monocyte-derived macrophages were treated with no 17␤-estradiol, physiologic levels (1 ؋ 10 ؊8 M) of 17␤-estradiol, or 1 ؋ 10 ؊8 M 17␤-estradiol followed by withdrawal of 17␤-estradiol. Surface expression of CD16 and CD16 messenger RNA was measured using fluorescence-activated cell sorting (FACS) and semiquantitative reverse transcription-polymerase chain reaction, respectively. Cytokine release from 17␤-estradiol-treated or untreated monocytes was then quantitated by enzyme-linked immunosorbent assay and FACS after crosslinking the receptor with anti-CD16 antibodies.Results. CD16 transcript significantly increased in macrophage-like THP-1 cells and in primary, peripheral blood macrophages in the absence of 17␤-estradiol, and the observed increase in message was dependent on transcription. CD16 receptor levels on CD14؉, transforming growth factor ␤-treated primary monocytes also increased in cells deprived of 17␤-estradiol. Analysis of the cytokines released showed that CD16 crosslinking stimulated significant increases in TNF␣, IL-1␤, and IL-6 due to the absence of estrogen.Conclusion. Estrogen can modulate proinflammatory cytokine release from activated monocytes and/or macrophages, in part through modulation of CD16 expression.

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“…FcRs present on synovial fibroblasts and extracellular matrix have been described previously (17)(18)(19)(20). To evaluate whether joint inflammation is associated with bone marrow-derived elements or with other connective tissues, bone marrow chimeras were made by irradiating C57BL/6 and Fc␥R recipients and reconstituting them with Fc␥R and C57BL/6 donor bone marrow, respectively.…”

Section: Adoptive Transfer Of Arthritis Is Dependent On Fcr On Bone Mmentioning

confidence: 99%

The Role of FcγR Signaling in the K/B × N Serum Transfer Model of Arthritis

Corr

Crain

2002

The Journal of Immunology

138

127

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Spontaneous arthritis in the KRN transgenic mouse (K/BxN) model is due to the autoreactivity of the transgenic TCR and subsequent induction of autoantibodies directed against glucose-6-phosphate isomerase. These autoantibodies transfer clinically apparent arthritis into most recipient mouse strains and systemic catabolism of the transferred Abs attenuates paw swelling. Although mice deficient in the common γ-chain of the FcγR did not show clinical synovitis after receiving K/BxN sera, erosive lesions in the bone still developed. Further analysis demonstrated that FcγRII−/− mice manifested accelerated arthritis whereas the FcγRIII−/− mice had a more slowly progressing arthritis. Paw swelling required FcγR expression by bone marrow-derived cells and mast cells substantially contributed to the acute phase of paw swelling. In the K/BxN serum transfer model of arthritis, there is a clinically apparent acute phase, which is modulated by FcγRII and FcγRIII, and a subacute component, which results in bone erosion, even in the absence of FcγR signaling.

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Differential distribution of FcγRIIIa in normal human tissues and co‐localization with DAF and fibrillin‐1: implications for imm_unological microenvironments

Cited by 59 publications

References 31 publications

Chronic graft-versus-host disease: clinical manifestation and therapy

Chronic graft-versus-host disease: clinical manifestation and therapy

17β‐estradiol regulates cytokine release through modulation of CD16 expression in monocytes and monocyte‐derived macrophages

The Role of FcγR Signaling in the K/B × N Serum Transfer Model of Arthritis

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