Inflammasomes cross-talk with lymphocytes to connect the innate and adaptive immune response

Zhang, Hongliang; Gao, Jie; Tang, Yujie; Jin, Tengchuan; Tao, Jin‐Hui

doi:10.1016/j.jare.2023.01.012

Cited by 12 publications

(8 citation statements)

References 147 publications

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“…IL-1β and IL-18 are crucial in the activation of the specific immune response: their production and release cause the release of an additional subset of cytokines from tissue cells by directing differentiation through stimulation of Th1, Th2, and Th17 populations. In this context, multiple studies suggest how IL-1β and IL-18 can act as a bridge between the innate and acquired immune response [72][73][74]. They can activate lymphocytes and increase T-and B-cell proliferation, stimulate natural killer cell activity and cytokine secretion, and contribute to T-cell proliferation, memory T-cell expansion, and dendritic cells.…”

Section: Discussionmentioning

confidence: 99%

Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1)

Caproni,

Nordi,

Fontana

et al. 2024

IJMS

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Although Herpes simplex virus type 1 (HSV-1) has been deeply studied, significant gaps remain in the fundamental understanding of HSV-host interactions: our work focused on studying the Infected Cell Protein 27 (ICP27) as an inhibitor of the Absent-in-melanoma-2 (AIM 2) inflammasome pathway, leading to reduced pro-inflammatory cytokines that influence the activation of a protective innate immune response to infection. To assess the inhibition of the inflammasome by the ICP27, hTert-immortalized Retinal Pigment Epithelial cells (hTert-RPE 1) infected with HSV-1 wild type were compared to HSV-1 lacking functional ICP27 (HSV-1∆ICP27) infected cells. The activation of the inflammasome by HSV-1∆ICP27 was demonstrated by quantifying the gene and protein expression of the inflammasome constituents using real-time PCR and Western blot. The detection of the cleavage of the pro-caspase-1 into the active form was performed by using a bioluminescent assay, while the quantification of interleukins 1β (IL-1β) and 18 (IL-18)released in the supernatant was quantified using an ELISA assay. The data showed that the presence of the ICP27 expressed by HSV-1 induces, in contrast to HSV-1∆ICP27 vector, a significant downregulation of AIM 2 inflammasome constituent proteins and, consequently, the release of pro-inflammatory interleukins into the extracellular environment reducing an effective response in counteracting infection.

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Section: Discussionmentioning

confidence: 99%

Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1)

Caproni,

Nordi,

Fontana

et al. 2024

IJMS

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“…Recently, the NLRP3 inflammasome has emerged as an important pathway to promote inflammatory properties in B-cells, such as IL-1β production [ 116 ]. Interestingly, its activation in B-cells is regulated by the BAFF system and BCR signalling [ 117 ], which makes this inflammasome a relevant putative mechanism by which B-cells could contribute to the inflammatory milieu observed in PAH.…”

Section: Effector Mechanisms Of B-cells In Pahmentioning

confidence: 99%

B-cells in pulmonary arterial hypertension: friend, foe or bystander?

Sanges,

Tian,

Dubucquoi

et al. 2024

Eur Respir J

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There is an unmet need for new therapeutic strategies that target alternative pathways to improve the prognosis of patients with pulmonary arterial hypertension (PAH). As immunity has been involved in the development and progression of vascular lesions in PAH, we review the potential contribution of B cells in its pathogenesis and evaluate the relevance of B cell-targeted therapies. Circulating B cell homeostasis is altered in PAH patients, with total B-cell lymphopenia, abnormal subset distribution (expansion of naïve and antibody-secreting cells, reduction of memory B cells) and chronic activation. B cells are recruited to the lungs through local chemokine secretion, and activated by several mechanisms: 1) interaction with lung vascular auto-antigens through cognate B cell receptors; 2) co-stimulatory signals provided by T follicular helper (Tfh) cells (IL-21), T helper 2 (Th2) cells and mast cells (IL-4, IL-6 and IL-13); and 3) increased survival signals provided by B cell activating factor (BAFF) pathways. This activity results in the formation of germinal centres within perivascular tertiary lymphoid organs and in the local production of pathogenic autoantibodies that target the pulmonary vasculature and vascular stabilization factors (including angiotensin-II/endothelin-1 receptors and bone morphogenetic protein receptors). B cells also mediate their effects through enhanced production of pro-inflammatory cytokines, reduced anti-inflammatory properties by regulatory B cells, IgG-induced complement activation, and IgE-induced mast cell activation. Precision-medicine approaches targeting B cell immunity are a promising direction for select PAH conditions, as suggested by the efficacy of anti-CD20 therapy in experimental models and a trial of rituximab in systemic sclerosis-associated PAH.

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“…The aforementioned impacts contribute positively to the host's capacity to resist specific pathogens [76]. IL-1β also mediates the cross-talk between innate and adaptive immunity [77].…”

Section: The Biological Functions Of Nlrp3 Inflammasomementioning

confidence: 99%

New Potentiality of Bioactive Substances: Regulating the NLRP3 Inflammasome in Autoimmune Diseases

Chen,

Wang,

Chen

2023

Nutrients

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The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is an essential component of the human innate immune system, and is closely associated with adaptive immunity. In most cases, the activation of the NLRP3 inflammasome requires priming and activating, which are influenced by various ion flux signals and regulated by various enzymes. Aberrant functions of intracellular NLRP3 inflammasomes promote the occurrence and development of autoimmune diseases, with the majority of studies currently focused on rheumatoid arthritis, systemic lupus erythematosus and systemic sclerosis. In recent years, a number of bioactive substances have shown new potentiality for regulating the NLRP3 inflammasome in autoimmune diseases. This review provides a concise overview of the composition, functions, and regulation of the NLRP3 inflammasome. Additionally, we focus on the newly discovered bioactive substances for regulating the NLRP3 inflammasome in autoimmune diseases in the past three years.

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Inflammasomes cross-talk with lymphocytes to connect the innate and adaptive immune response

Cited by 12 publications

References 147 publications

Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1)

Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1)

B-cells in pulmonary arterial hypertension: friend, foe or bystander?

New Potentiality of Bioactive Substances: Regulating the NLRP3 Inflammasome in Autoimmune Diseases

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