Intracellular IL-1 alpha in fibroblasts as a possible endogenous mediator of joint damage in rheumatoid arthritis

R. N. Apte

Intracellular IL-1 alpha in fibroblasts as a possible endogenous mediator of joint damage in rheumatoid arthritis

R. N. Apte

The Shraga Segal Department of Microbiology, Immunology and Genetics

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Interleukin-1 (IL-1) and tumor necrosis factor α (TNFα) are the most potent pro-inflammatory cytokines. Acting in synergy, they mediate many consequences of inflammatory responses. IL-1 consists of a family of two proteins, namely IL-1α and IL-1β. It is shown that fibroblasts display a unique pattern of IL-1 expression. Under inflammatory conditions, fibroblasts display inductive patterns of IL-1α bioactivity.

Original language	English
Pages (from-to)	285-288
Number of pages	4
Journal	Israel Journal of Medical Sciences
Volume	33
Issue number	4
State	Published - 1 Apr 1997

Keywords

Fibroblasts
Rheumatoid arthritis

ASJC Scopus subject areas

Bioengineering

Cite this

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abstract = "Interleukin-1 (IL-1) and tumor necrosis factor α (TNFα) are the most potent pro-inflammatory cytokines. Acting in synergy, they mediate many consequences of inflammatory responses. IL-1 consists of a family of two proteins, namely IL-1α and IL-1β. It is shown that fibroblasts display a unique pattern of IL-1 expression. Under inflammatory conditions, fibroblasts display inductive patterns of IL-1α bioactivity.",

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AB - Interleukin-1 (IL-1) and tumor necrosis factor α (TNFα) are the most potent pro-inflammatory cytokines. Acting in synergy, they mediate many consequences of inflammatory responses. IL-1 consists of a family of two proteins, namely IL-1α and IL-1β. It is shown that fibroblasts display a unique pattern of IL-1 expression. Under inflammatory conditions, fibroblasts display inductive patterns of IL-1α bioactivity.

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Intracellular IL-1 alpha in fibroblasts as a possible endogenous mediator of joint damage in rheumatoid arthritis

Abstract

Keywords

ASJC Scopus subject areas

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