The role of IL-23 and CCR6+ memory T helper cells in healthy and inflammatory arthritis conditions

Research output: Types of ThesisDoctoral ThesisInternal

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Abstract

Interleukin 23 (IL-23) is a pro-inflammatory cytokine, which is secreted by activated
dendritic cells and macrophages, which are located in peripheral tissues such as the
intestinal mucosa, skin and the joints. Once secreted, IL-23 binds to the IL-23 receptor
(IL-23R) on its target cells to induce the production of other pro-inflammatory cytokines,
such as IL-17A, IL-22, TNFα. These cytokines can also stimulate the production of other
pro-inflammatory cytokines, anti-microbial peptides and chemokines, for instance for
control of infections.
In addition to its contribution in fighting pathogens that can cause infections, IL-23
can also affect bone remodeling during physiological condition. This is made possible
through (in)direct interactions of IL-23 with several immune and non-immune cells,
such as osteoblasts (bone forming cells) and osteoclasts (bone resorbing cells).

This thesis consists of two parts. In part I, we focused on the effects of IL-23/IL-23R
signaling under healthy conditions on CCR6+ memory T helper (Th) cells, one of the
target cells of IL-23, and the precursors of osteoclasts (chapter 4). Also, the role of IL-23R signaling was investigated in physiological bone remodeling (chapter 3).

In part II, the focus was on the role of IL-23/IL-23R signaling and its target cells, the
CCR6+ Th cells, during inflammatory arthritis (IA). Inflammatory arthritis is a broad
term used for several conditions in which an abnormal immune response leads to joint
inflammation. This thesis focuses on rheumatoid arthritis (RA) and psoriatic arthritis
(PsA)
Original languageEnglish
Awarding Institution
  • Erasmus University Rotterdam
Supervisors/Advisors
  • Lubberts, Erik, Supervisor
  • Hazes, Mieke, Supervisor
Award date5 Jul 2024
Place of PublicationRotterdam
Print ISBNs978-94-6469-902-9
Publication statusPublished - 5 Jul 2024

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