Der p 2 can induce bystander activation of B cells derived from patients with systemic lupus erythematosus

Yu, Shyr-Shen; Liao, En-Chih; Tsai, Jaw‐Ji

doi:10.1016/j.imbio.2014.07.018

Cited by 7 publications

(6 citation statements)

References 45 publications

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“…This type of activation is mediated by indirect signals from the inflammatory environment, including co-signaling receptors ligands, cytokines, chemokines, pathogen-associated molecular patterns, and extracellular vesicles with microbial particles (Figure 2A) [110]. Bystander activation has been linked to the development or recurrence of various autoimmune diseases, such as rheumatoid arthritis [111], lupus erythematosus [112], multiple sclerosis [113], and autoimmune thyroid diseases [114]. Cytokines produced in the inflammatory microenvironment activate bystander T cells to secrete IL-2, IL-6, and TNF-α, perpetuating the inflammatory environment and forming a vicious cycle [115].…”

Section: Bystander Activationmentioning

confidence: 99%

Autoimmunity: A New Focus on Nasal Polyps

Huang

2023

IJMS

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Chronic rhinosinusitis with nasal polyps (CRSwNP) has long been considered a benign, chronic inflammatory, and hyperplastic disease. Recent studies have shown that autoimmune-related mechanisms are involved in the pathology of nasal polyps. Activated plasma cells, eosinophils, basophils, innate type 2 lymphocytes, mast cells, and proinflammatory cytokine in polyp tissue indicate the mobilization of innate and adaptive immune pathways during polyp formation. The discovery of a series of autoantibodies further supports the autoimmune nature of nasal polyps. Local homeostasis dysregulation, infection, and chronic inflammation may trigger autoimmunity through several mechanisms, including autoantigens overproduction, microbial translocation, molecular mimicry, superantigens, activation or inhibition of receptors, bystander activation, dysregulation of Toll-Like Receptors (TLRs), epitope spreading, autoantigens complementarity. In this paper, we elaborated on the microbiome-mediated mechanism, abnormal host immunity, and genetic changes to update the role of autoimmunity in the pathogenesis of chronic rhinosinusitis with nasal polyps.

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Section: Bystander Activationmentioning

confidence: 99%

Autoimmunity: A New Focus on Nasal Polyps

Huang

2023

IJMS

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“…Our previous study showed that the Group 2 major allergen of Dermatophagoides pteronyssinus (Dp2) can induce inflammasome activation through autoantigen/ Autoantibody production by B cells, and that this autoantigen/ autoantibody production was not down regulated by siRNA NLRP3 [17,18]. It will be of importance to investigate other family members of inflammasome, particularly AIM2.…”

Section: Dp2-induced Autoantigen/autoantibody Production From Patientmentioning

confidence: 99%

Dp2-Induced Autoantigen/Autoantibody Production From Patients With Systemic Lupus Erythematosus Is Done Through AIM2 And Not NLRP3

Tsai¹

2017

JRAD

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Systemic Lupus Erythematosus (SLE) is a disease characterized by the production of autoantibodies against different autoantigens, including double stranded DNA (dsDNA). AIM2 (Protein absent in melanoma 2) is one of the inflammasome proteins which can directly bind to dsDNA. It is therefore possible to speculate that AIM2 may contribute to the disease development of SLE. B cell lines obtained from patients with Dp-allergic SLE were used to investigate the involvement of AIM2 in autoantibody production. The obtained B cells were then cultured with Dp2 for inflammasome activation. The cells-cultured pellet and supernatant were subsequently collected for the measurement of autoantigens, autoantibodies and inflammatory cytokines. The inflammasome of AIM2 and NLRP3 was measured and correlated with autoantibodies production. The B cells were pretreated with siRNA of AIM2, followed by Dp2 stimulation to confirm the activation of AIM2. The results showed that Dp2 could induce inflammasome activation with an increased expression of both NLRP3 and AIM2, which was associated with the production of TRIM-21/PGK1, anti-TRIM21/anti-PGK-1 and IL8/IL-1β. In the siRNA AIM2 study, Dp2 induced autoantigen/autoantibody/cytokine production could be down-regulated by siRNA in association with a decreased expression of AIM2. Dp2-induced expression of NLRP3 and AIM2 can both be down-regulated by CPP ECP. In Conclusion: Dp2 induced expression of NLRP3 and AIM2 is associated with autoantigen and autoantibody production from B cells derived from Dp-allergic SLE. These autoantigens/autoantibodies can be downregulated only by siRNA AIM2, and not by NLRP3.

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“…The group 2 antigen of Dermatophagoides pteronyssinus (Dp2) is one of the major Dp allergens, which has been reported to cause IgE immune responses in the majority of allergic patients. Dp2 can induce bystander activation of B cells to generate autoantigens and stimulate production of autoanitbodies in Dp-sensitive SLE patients [6].…”

Section: Introductionmentioning

confidence: 99%

Dp2-induced autoantigen/autoantibody production from patients with systemic lupus erythematosus is not affected by AhR agonist

Yin¹,

Chang²,

Tsai³

2020

J Transl Sci

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Systemic Lupus Erythematosus (SLE) is a multifactorial systemic autoimmune disorder that can produce numerous abnormalities in cellular and humoral immune responses, including abnormal autoantigen and autoantibody production by dysregulated B cells. There are many known ligands of the AhR (aryl hydrocarbon receptor) in air pollutants, such as 6-formylindolo[3,2-b] Carbazole (FICZ) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). This study investigated the effect of FICZ/TCDD on the autoantigen/autoantibody and inflammatory cytokine production of B cells in Dp-allergic SLE. Dp2-induced autoantigen/autoantibody from B cell lines and PBMC derived from Dp-allergic SLE were used to evaluate the effects of FICZ/TCDD. Autoantigen/autoantibody and inflammatory cytokines were measured after cells were stimulated with FICZ/TCDD in conjuction with Dp2. The results showed that both FICZ/TCDD can activate AhR expression and induce the mRNA expression of IL-8. There were no effects on the production of IFN-α, IL-6, or autoantigen/autoantibody, except enolase-1. In the presence of Dp2 there were no augmentation effects of FICZ/TCDD on the expression of AhR or any of the autoantigens/autoantibodies from B cell lines. Although Dp2 could induce IL-8 production from PBMC derived from Dp-allergic SLE and non-SLE patients, there were no differences between the two groups and FICZ also showed no augmentation effects on IL-8 production. In conclusion, although FICZ/TCDD can induce AhR expression and IL-8 production from B cells derived from Dp-allergic SLE. There were no augmentation effects on Dp2-induced autoantigen/autoantibody or inflammatory cytokine production by FICZ/TCDD. In the presence of Dp2, FICZ had no augmentation effect on IL-8 production from PBMC derived from patients with Dp-allergic SLE.

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Der p 2 can induce bystander activation of B cells derived from patients with systemic lupus erythematosus

Cited by 7 publications

References 45 publications

Autoimmunity: A New Focus on Nasal Polyps

Autoimmunity: A New Focus on Nasal Polyps

Dp2-Induced Autoantigen/Autoantibody Production From Patients With Systemic Lupus Erythematosus Is Done Through AIM2 And Not NLRP3

Dp2-induced autoantigen/autoantibody production from patients with systemic lupus erythematosus is not affected by AhR agonist

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