S1P1 receptor antagonists Fingolimod and SEW2871 affect human group 1 and 3 innate lymphoid cell biology
Author(s): ,
A. Eken
Affiliations:
Medical Biology
,
M.F. Yetkin
Affiliations:
Neurology
,
F.Z. Okus
Affiliations:
Medical Biology
,
S. Erdem
Affiliations:
Medical Biology
,
M. Cakir
Affiliations:
Medical Biology
,
M.S. Kutuk
Affiliations:
Gynecology
,
A. Vural
Affiliations:
Ear Nose Throat, Erciyes University
,
I. Kara
Affiliations:
Ear Nose Throat, Erciyes University
,
H. Donmez Altuntas
Affiliations:
Medical Biology
,
M. Mirza
Affiliations:
Neurology, ErciyesUniversity, Kayseri, Turkey
H. Canatan
Affiliations:
Medical Biology
ECTRIMS Online Library. Yetkin M. 10/11/18; 228605; P762
Mehmet Fatih Yetkin
Mehmet Fatih Yetkin
Contributions
Abstract

Abstract: P762

Type: Poster Sessions

Abstract Category: Pathology and pathogenesis of MS - Immunology

Sphingosine 1 phosphate receptor is expressed by lymphocytes and regulates their egress from secondary lymphoid organs. Innate lymphoid cell (ILC) family have been expanded with the discovery of group 1,2 and 3 ILCs, namely ILC1, ILC2 and ILC3. ILC3 and ILC1 have remarkable similarity to helper CD4+ T cell lineage members Th17 and Th1, which are important in multiple sclerosis pathology. Whether human ILC subsets express S1P1 or respond to its antagonists have not been studies. In this study, we used peripheral blood/cord blood and tonsil lymphocytes as a source of human ILCs. We show that human ILCs express S1P1 receptor mRNA and protein. Comparison of peripheral blood ILC number between Fingolimod-receiving and non-receiving Multiple sclerosis patients revealed that ILCs respond to Fingolimod, an S1P1 agonist, and causes ILC-penia in circulation. Importantly, ex vivo exposure of ILC3 and ILC1 to Fingolimod or SEW2871, another S1P1 antagonist, reduces production of ILC3 and ILC1 associated cytokines GM-CSF, IL-22, IL-17 and IFN-g respectively. To our knowledge, this is the first study to investigate the impact of Fingolimod on human ILC subsets in vivo and ex vivo.
Disclosure: Ahmet Eken: nothing to disclose, Mehmet Fatih Yetkin: nothing to disclose, Fatma Zehra Okus:nothing to disclose, Serife Erdem:nothing to disclose, Mustafa Cakir :nothing to disclose, M.Serdar Kutuk:nothing to disclose,Alperen Vural :nothing to disclose, Irfan Kara :nothing to disclose, Hamiyet Donmez Altuntas :nothing to disclose, Meral Mirza :nothing to disclose, Halit Canatan:nothing to disclose

Abstract: P762

Type: Poster Sessions

Abstract Category: Pathology and pathogenesis of MS - Immunology

Sphingosine 1 phosphate receptor is expressed by lymphocytes and regulates their egress from secondary lymphoid organs. Innate lymphoid cell (ILC) family have been expanded with the discovery of group 1,2 and 3 ILCs, namely ILC1, ILC2 and ILC3. ILC3 and ILC1 have remarkable similarity to helper CD4+ T cell lineage members Th17 and Th1, which are important in multiple sclerosis pathology. Whether human ILC subsets express S1P1 or respond to its antagonists have not been studies. In this study, we used peripheral blood/cord blood and tonsil lymphocytes as a source of human ILCs. We show that human ILCs express S1P1 receptor mRNA and protein. Comparison of peripheral blood ILC number between Fingolimod-receiving and non-receiving Multiple sclerosis patients revealed that ILCs respond to Fingolimod, an S1P1 agonist, and causes ILC-penia in circulation. Importantly, ex vivo exposure of ILC3 and ILC1 to Fingolimod or SEW2871, another S1P1 antagonist, reduces production of ILC3 and ILC1 associated cytokines GM-CSF, IL-22, IL-17 and IFN-g respectively. To our knowledge, this is the first study to investigate the impact of Fingolimod on human ILC subsets in vivo and ex vivo.
Disclosure: Ahmet Eken: nothing to disclose, Mehmet Fatih Yetkin: nothing to disclose, Fatma Zehra Okus:nothing to disclose, Serife Erdem:nothing to disclose, Mustafa Cakir :nothing to disclose, M.Serdar Kutuk:nothing to disclose,Alperen Vural :nothing to disclose, Irfan Kara :nothing to disclose, Hamiyet Donmez Altuntas :nothing to disclose, Meral Mirza :nothing to disclose, Halit Canatan:nothing to disclose

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