PhD Scientific Days 2026

Poster Session 1.A - Molecular Medicine

Investigating the role of β2-integrins in in vitro and in vivo inflammatory reactions

Name of the presenter

Papp, Zsuzsanna

Institute/workplace of the presenter

Department of Physiology

Authors

Zsuzsanna Papp¹, Dorottya Deli¹, Attila Mócsai¹
1: Department of Physiology

Text of the abstract

Neutrophil granulocytes express β2 integrins, such as LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18), which regulate adhesion-dependent processes including cytoskeletal rearrangement, gene expression, and cell differentiation. Although these molecules are implicated in autoimmune inflammation, their precise roles remain unclear.

This study aimed to define the contributions of LFA-1 and Mac-1 in inflammatory responses using both in vitro and in vivo approaches. Bone marrow chimeric mice were generated by transplanting cells from wild-type (WT), CD11a-deficient (LFA-1 KO), CD11b-deficient (Mac-1 KO), or CD18-deficient (CD18 KO) donors into irradiated WT recipients. Neutrophil surface expression of integrins was confirmed by flow cytometry. Inflammation was assessed using the K/BxN serum-transfer arthritis model, with disease progression monitored macroscopically. Additional analyses included flow cytometric assessment of peripheral blood cells, as well as measurements of neutrophil superoxide production and migration.

WT chimeras developed severe arthritis, whereas CD18 KO chimeras showed almost complete protection, highlighting the essential role of CD18. LFA-1 KO mice were partially protected, especially at lower serum doses, while Mac-1 KO mice exhibited slightly more severe disease. Functionally, CD18 and Mac-1 deficiency reduced adhesion-dependent superoxide release, whereas LFA-1 deficiency impaired neutrophil migration.

In conclusion, CD18 is critical for inflammatory responses, but LFA-1 and Mac-1 have distinct roles. LFA-1 primarily mediates neutrophil migration and arthritis development, while Mac-1 is more involved in adhesion-dependent oxidative responses.

Funding: Hungarian National Research, Development and Innovation Office (TKP2021-EGA-24 and TKP2021-EGA-29), the HUN-REN Hungarian Research Network (0207007) and the Hungarian Academy of Sciences (LP2024-16/2024).