Lazaros I. Sakkas (Greece)
Lazaros I. Sakkas, MD, DM, PhD (UK), FRCP (UK)(Hon) Professor Emeritus, University of Thessaly, Larissa, Greece Adjunct Assistant Professor, Temple University School of Medicine, Philadelphia, PA, USA, Adjunct Professor, Old dominion University, Norfolk, VA, USA Professor L Sakkas received his medical degree and his DM degree form the national and Kapodistrian University of Athens, and specialized in internal medicine in Athens, and in Rheumatology at Guy’s Hospital, London. Dr Sakkas has extensive experience in bench reseach working on the HLA and other genetic associations of rheumatic diseases for his PhD degree in London, and then working on T cell involvement in osteoarthritis and systemic sclerosis at Temple University, Philadelphia, USA. He has also extensive clinical experience in different clinical environments in London, Philadelphia and Larissa. In Larissa, as a Professor and Medicine and Rheumatology, he organized the Rheumatology Service of the new University General Hospital of Larissa and worked on B cells in systemic sclerosis and on the infectious basis of autoimmune diseases. He served as Editor and Editorial member in a few journals and as a Reviewer in many journals and published over 240 Greek and English language papers and over 16 English language book chapters.

Moderator of 1 Session

 Congress Calendar

PARALLEL SESSION 20 - MYOSITIS (MUSCLES)

Date
Mon, 13.06.2022
Session Time
10:30 - 12:30
Room
NIKOS SKALKOTAS
Session Type
PARALLEL SESSIONS
Chair(s)

Presenter of 1 Presentation

 Congress Calendar

IS002 - SYSTEMIC SCLEROSIS: FROM BENCH TO BEDSIDE (ID 780)

Date
Tue, 28.02.2023
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Session Name
0040 - PLENARY SESSION 01 (ID 7)
Lecture Time
09:10 - 09:35
Presenter

Abstract

Abstract Body

Systemic scletosis (SSc) is a complex disease characterized by extensive collagen deposition, microvasculopathy and many autoantibodies (autoAbs). Activation of fibroblasts, a prerequisite for collagen production, can be cause vis various stimuli, including TGFβ, IL-6, and PDGF. T cells and B cells are likely inducers of fibroblast activation.

Tcells are oligoclonal in SSc skin lesions and peripheral blood(PB) and are of profibrotic TH2 type, whereas regulatory T cells (Tregs) are impaired. Cytotoxic CD4+Tcells in skin lesions can induce endothelial cell apoptosis. Effector B cells are hyperactivated whereas IL-10-producing regulatory B cells are decreased. B cells can cause fibrosis through interaction with fibroblasts, macrophages and dendritic cells, and through autoabs, many of which have promote fibrosis. In addition, B cells with high affinity for DNA-topoisomerase I(topo I) produce IL-6 and cause fibrosis, whereas low affinity B cells for topo I produce IL-10 and inhibit fibrosis in a mouse SSc model. Ibrutinib, a Bruton’s tyrosine kinase inhibitor, promoted low affinity B cells for topo I in SSc patients and inhibited fibrosis in a mouse SSc model. Induction ot Tregs with low-dose IL-2 administration and JAK/STAT pathway inhibition in SSc mice ameliorated fibrosis.

Many of these bench findings find application as current therapeutic approaches in human SSc and others, such as administration of ibrutinib, as potential therapeutic agents

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