T Regulatory Cells and TH17 Cells in Peri–Silicone Implant Capsular Fibrosis

Wolfram, Dolores; Rabensteiner, Evelyn; Grundtman, Cecilia; Böck, Günther; Mayerl, Christina; Parson, Walther; Almanzar, Giovanni; Hasenöhrl, Carlo; Piza‐Katzer, Hildegunde; Wick, Georg

doi:10.1097/prs.0b013e31823aeacf

Cited by 134 publications

(112 citation statements)

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“…For example, Sakaki et al (28) showed elevated numbers of intrahepatic Tregs in patients with autoimmune liver diseases as well as in patients with viral hepatitis. As detailed below, our group has demonstrated an inverse correlation between the numbers of Tregs in the perisilicone mammary implant-connected capsular tissue and the severity of fibrosis (29). These contradictory findings of Treg involvement in fibrosis may be explained by the (im)balance between the degree of inflammatory response suppression and TGF-β1 production.…”

Section: Regulatory Mechanisms-t Regulatory Cells and Fibrosismentioning

confidence: 92%

The Immunology of Fibrosis

Wick¹,

Grundtman²,

Mayerl³

et al. 2013

Annu. Rev. Immunol.

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288

277

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Fibrosis is the production of excessive amounts of connective tissue, i.e., scar formation, in the course of reactive and reparative processes. Fibrosis develops as a consequence of various underlying diseases and presents a major diagnostically and therapeutically unsolved problem. In this review, we postulate that fibrosis is always a sequela of inflammatory processes and that the many different causes of fibrosis all channel into the same final stereotypical pathways. During the inflammatory phase, both innate and adaptive immune mechanisms are operative. This concept is exemplified by fibrotic diseases that develop as a consequence of tissue damage, primary inflammatory diseases, fibrotic alterations induced by foreign body implants, "spontaneous" fibrosis, and tumor-associated fibrotic changes.

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Section: Regulatory Mechanisms-t Regulatory Cells and Fibrosismentioning

confidence: 92%

The Immunology of Fibrosis

Wick¹,

Grundtman²,

Mayerl³

et al. 2013

Annu. Rev. Immunol.

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288

277

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“…Wolfram et al suggested that a specific antigen-driven local immune response, involving activated Th1/Th17 cells, is triggered by silicone implants. T cells around the silicone capsule tend to synthesize interleukin-17, interleukin-6, interleukin-8, and other growth factors [22]. The resultant peri-capsular fibrosis is promoted by the production of pro-fibrotic cytokines.…”

Section: Silicone As An Adjuvant In Asiamentioning

confidence: 99%

Autoimmune/inflammatory syndrome induced by adjuvant (ASIA) evolution after silicone implants. Who is at risk?

2015

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Silicone implants have been in use since the mid-twentieth century, especially in the field of reconstructive breast surgery, and have long been considered as biologically inert and harmless. However, growing body of evidence from the past two decades links silicone with subsequent autoimmunity-related complications, collectively known as autoimmune/inflammatory syndrome induced by adjuvant--ASIA. Previous data suggest that while some patients tend to develop post-exposure autoimmune phenomena such as ASIA, other do not. However, thus far, no criteria for risk stratification were suggested. This current review summarizes the data linking silicone implants and autoimmunity, suggesting means of defining individuals who are at increased risk to develop silicone-induced ASIA, and therefore, a recommendation was made to avoid silicone implantation, e.g., individuals with previously diagnosed autoimmune disorders or with genetic preponderance for hyperactive immune system should not be considered as candidates for silicone implantation.

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“…With only local inflammatory components considered relevant to the FBR, direct correlation of implant responses with systemic immune pathologies was difficult to connect. Preclinical and clinical observations noted the presence of T cells with implants but their relevance to the fibrotic inflammatory response was unclear [14,45]. Here we present evidence of an IL17 inflammatory response and cellular senescence in the FBR to biomaterials and implicate them in the associated fibrotic response.…”

Section: Discussionmentioning

confidence: 55%

“…The TH2 T effector cells responding to proregenerative biological scaffolds secrete interleukin 4 (IL4) and direct the function of macrophages to promote muscle repair [13]. The presence of T cells has been recognized in the FBR in animal models and surrounding clinical implants but their nature, activation status and role in the response is still largely unknown [10,14]. Adaptive responses that depend on T cells, which conventionally recognize MHC-presented peptide antigens, have not been seriously considered in the response to synthetic materials despite their increasing association with fibrotic disease [15][16][17].…”

Section: Main Textmentioning

confidence: 99%

Interleukin-17 and senescence regulate the foreign body response

Chung

Maestas

Lebid

et al. 2019

Preprint

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AbstractSynthetic biomaterials and medical devices suffer to varying levels from fibrosis via the foreign body response (FBR). To explore mechanistic connections between the immune response and fibrosis from the FBR, we first analyzed fibrotic capsule surrounding human breast implants and found increased numbers of interleukin (IL)17-producing γδ+T cells and CD4+TH17 cells as well as senescent cells. Further analysis in a murine model demonstrated an early innate IL17 response to synthetic implants, mediated by innate lymphoid cells and γδ+T cells, was followed by a chronic adaptive antigen dependent CD4+TH17 cell response. Mice deficient in IL17 signaling established that IL17 was required for the fibrotic response to materials and the development of p16INK4asenescent cells. Treatment with a senolytic agent reduced IL17 expression and fibrosis. Discovery of a feed-forward loop between the TH17 and senescence response to synthetic materials introduces new targets for therapeutic intervention in the foreign body response.

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T Regulatory Cells and TH17 Cells in Peri–Silicone Implant Capsular Fibrosis

Cited by 134 publications

References 0 publications

The Immunology of Fibrosis

The Immunology of Fibrosis

Autoimmune/inflammatory syndrome induced by adjuvant (ASIA) evolution after silicone implants. Who is at risk?

Interleukin-17 and senescence regulate the foreign body response

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