Expressão de proteínas reguladoras do complemento CD55, CD59, CD35 e CD46 na artrite reumatoide

Piccoli, Amanda Kirchner; Alegretti, Ana Paula; Schneider, Laiana; Lora, Priscila Schmidt; Xavier, Ricardo Machado

doi:10.1590/s0482-50042011000500009

Cited by 18 publications

(5 citation statements)

References 59 publications

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“…In a similar way to CD21 and CD32, CD35 is also related to some autoimmune diseases [34,35]. It had been shown that soluble recombinant CD35 improves inflammation, demyelination, and severity of clinical disease in a rat model of MS disease [36].…”

Section: Discussionmentioning

confidence: 99%

Cytometric profiling in various clinical forms of multiple sclerosis with respect to CD21+, CD32+, and CD35+ B and T cells

Zandieh

Izad

Fakhri

et al. 2013

Transl Neurodegener

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BackgroundWe aimed to evaluate the frequency of various types of B and T cells expressing CD21, CD32, and CD35 in multiple sclerosis (MS) clinical courses.MethodsPeripheral blood mononuclear cell from 30 MS patients (17 relapsing remitting [RRMS], six secondary progressive [SPMS], and seven primary progressive MS [PPMS]) and 18 healthy subjects were analyzed. All patients were in acute attack. Healthy controls were matched for age and gender ratio. The frequencies of various subsets of B and T cells were determined using flow cytometry.ResultsThe frequency of CD4+T cells was lower in MS patients compared to control subjects (41.14 ± 9.45% vs. 46.88 ± 6.98%, respectively, P < 0.05). The CD32+ fraction of CD4+T cells and the CD21+ fraction of CD8+T cells were higher in MS patients (2.85 ± 3.72% vs. 1.06 ± 0.62% for CD32+CD4+T cells, 2.71 ± 1.86% vs. 1.16 ± 0.99% for CD21+CD8+T cells in MS patients and control subjects, respectively, P < 0.05). After dividing subjects by type of MS course, higher values of these two T cell subsets were found in SPMS patients compared to control subjects (P < 0.05). Further, RRMS patients had lower levels of CD32+CD4+T cells than SPMS patients and also they had lower levels of CD32+CD8+T cells than PPMS patients (P < 0.05). However, neither the expression of CD35 on T cells nor the various B cell subsets were statistically different between the compared groups.ConclusionsOur findings demonstrate that T cell subsets expressing CD21 and CD32 may differ with respect to the presence or clinical forms of MS disease. By contrast, CD35+T cells and different subsets of B cells are not altered in various MS clinical courses.

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Section: Discussionmentioning

confidence: 99%

Cytometric profiling in various clinical forms of multiple sclerosis with respect to CD21+, CD32+, and CD35+ B and T cells

Zandieh

Izad

Fakhri

et al. 2013

Transl Neurodegener

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“…Signaling induced by CD46 activation may also regulate the Notch pathway, affecting not only the integrity of epithelial cells [230] but also immune function regulation. In the case of some chronic autoimmune diseases, the cofactor CD46 plays a significant role in regulation of the complement system and its synthesis has been found to be positively regulated by CRP [231,232].…”

Section: Wound Healingmentioning

confidence: 99%

Modeling of the immune response in the pathogenesis of solid tumors and its prognostic significance

2020

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Background Tumor initiation and subsequent progression are usually long-term processes, spread over time and conditioned by diverse aspects. Many cancers develop on the basis of chronic inflammation; however, despite dozens of years of research, little is known about the factors triggering neoplastic transformation under these conditions. Molecular characterization of both pathogenetic states, i.e., similarities and differences between chronic inflammation and cancer, is also poorly defined. The secretory activity of tumor cells may change the immunophenotype of immune cells and modify the extracellular microenvironment, which allows the bypass of host defense mechanisms and seems to have diagnostic and prognostic value. The phenomenon of immunosuppression is also present during chronic inflammation, and the development of cancer, due to its duration, predisposes patients to the promotion of chronic inflammation. The aim of our work was to discuss the above issues based on the latest scientific insights. A theoretical mechanism of cancer immunosuppression is also proposed. Conclusions Development of solid tumors may occur both during acute and chronic phases of inflammation. Differences in the regulation of immune responses between precancerous states and the cancers resulting from them emphasize the importance of immunosuppressive factors in oncogenesis. Cancer cells may, through their secretory activity and extracellular transport mechanisms, enhance deterioration of the immune system which, in turn, may have prognostic implications.

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“…In systemic lupus erythematosus (SLE) patients, mCD46 expression was found to be downregulated during lymphopenia and neutropenia relative to that in healthy subjects, whereas disease severity was associated with activation of the complement system 13–15 . In addition, decreased CD46 expression was associated with aggravation of the clinical symptoms of rheumatoid arthritis 16–18 .…”

Section: Introductionmentioning

confidence: 99%

Dysregulation of mCD46 and sCD46 contribute to the pathogenesis of bullous pemphigoid

Qiao

Dang

Cao

et al. 2017

Sci Rep

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Bullous pemphigoid (BP) is an autoimmune bullous disease caused by autoantibodies against BP180 in the epidermal basement membrane. Autoantibody-mediated complement activation is an important process in BP pathogenesis. CD46, a crucial complement regulatory protein in the complement activation, has been reported to be involved in several autoimmune diseases. In the present study, we investigated whether CD46 plays a role in BP development. We found that sCD46 expression was significantly increased in the serum and blister fluids of BP patients and correlated with the levels of anti-BP180 NC16A antibody and C3a. Otherwise, the level of mCD46 was decreased in lesions of BP patients, whereas the complement activation was enhanced. We also found that CD46 knockdown in HaCaT human keratinocytes enhanced autoantibody-mediated complement activation. Importantly, exogenous CD46 blocked complement activation in both healthy skin sections and keratinocytes induced by exposure to pathogenic antibodies from BP patients. These data suggest that CD46 deficiency is an important factor in BP pathogenesis and that increasing CD46 levels might be an effective treatment for BP.

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Expressão de proteínas reguladoras do complemento CD55, CD59, CD35 e CD46 na artrite reumatoide

Cited by 18 publications

References 59 publications

Cytometric profiling in various clinical forms of multiple sclerosis with respect to CD21+, CD32+, and CD35+ B and T cells

Cytometric profiling in various clinical forms of multiple sclerosis with respect to CD21+, CD32+, and CD35+ B and T cells

Modeling of the immune response in the pathogenesis of solid tumors and its prognostic significance

Dysregulation of mCD46 and sCD46 contribute to the pathogenesis of bullous pemphigoid

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