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The Pyrazole Derivative BTP2 Attenuates IgG Immune Complex-induced Inflammation
Georgios Sogkas1,2, Eduard Rau3, Faranaz Atschekzei3
1Division of Immunology and Rheumatology, Hannover Medical School, Hannover, Germany. sogkas.georgios@mh-hannover.de.
Inflammation
|August 31, 2017
Summary
Store-operated calcium entry (SOCE) is crucial for immune cell function. Inhibiting SOCE with BTP2 effectively reduced immune complex-mediated inflammation in mouse models, suggesting therapeutic potential for autoimmune diseases.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Store-operated calcium entry (SOCE) is a primary calcium influx pathway in non-excitable cells, including immune cells.
- STIM isoforms mediate SOCE and Fc receptor (FcR)-driven activation in macrophages and mast cells, relevant in allergic reactions and antibody-dependent tissue injury.
- SOCE presents a potential therapeutic target for immune complex (IC)-mediated autoimmunity and allergic asthma.
Purpose of the Study:
- To investigate the effect of the SOCE inhibitor BTP2 on Fc gamma receptor (FcγR) signaling and IC-induced tissue injury.
- To evaluate BTP2's therapeutic potential in models of IC-mediated inflammation.
Main Methods:
- BTP2 was used to inhibit SOCE in primary macrophages.
- FcγR-mediated responses were assessed in vitro.
- Reverse passive Arthus reaction was induced in mice (skin and lungs) to model IC-mediated tissue injury.
- Mice were treated with BTP2 or a control.
Main Results:
- BTP2 potently inhibited SOCE in primary macrophages, blocking FcγR-mediated responses.
- BTP2 treatment significantly attenuated inflammation in both the skin and lungs following IC-induced injury.
- These findings demonstrate the involvement of SOCE in FcγR-mediated responses.
Conclusions:
- SOCE plays a significant role in FcγR-mediated immune responses.
- BTP2 effectively inhibits SOCE and reduces IC-mediated inflammation in vivo.
- BTP2 shows therapeutic promise for treating IC-mediated autoimmune conditions.
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