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TITLEUnexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17AUTHOR(s)Anil Kumar Jaiswal, Mohanraj Sadasivam, Abdel Rahim A HamadCITATIONJaiswal AK, Sadasivam M, Hamad ARA. Unexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17. World J Diabetes 2018; 9(12): 220-225URLhttps://www.wjgnet.com/1948-9358/full/v9/i12/220.htmDOIhttps://dx.doi.org/10.4239/wjd.v9.i12.220OPEN ACCESSThis is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/CORE TIPCore tip: Interleukin-17 (IL-17) is a potent proinflammatory cytokine that plays a critical role in host defense against fungi and extracellular bacteria. Excessive production of IL-17, howeve r , h a s b e e n i m p l i c a t e d i n p a t h o g e n e s i s o f m a n y a u t o i m m u n e d i s e a s e s . O u r r e c e n t f i n d i n g s s h o w t h a t n a t u r a l k i l l e r T ( N K T ) c e l l s a n d T c e l l s e m p l o y s y n d e c a n - 1 ( s d c 1 ) , a h e p a r a n s u l f a t e p r o t e o g l y c a n t h a t i s p r e d o m i n a n t l y e x p r e s s e d b y e p i t h e l i a , t o p r e v e n t o u t o f c o n t r o l e x p a n s i o n o f I L - 1 7 - p r o d u c i n g s u b s e t s o f N K T ( N K T 1 7 ) c e l l a n d ( T 1 7 ) c e l l s . I n t h i s m i n i - r e v i e w , w e h i g h l i g h t t h e s e f i n d i n g s a n d b r i e f l y d i s c u s s t h e i r s i g n i f i c a n c e f o r d e v e l o p i n g n e w s t r a t e g i e s t o p r e v e n t I L - 1 7 - m e d i a t e d a u t o i m m m e d i s e a s e s . K E Y W O R D S N a t u r a l k i l l e r T c e l l ; N a t u r a l k i l l e r T 1 7 c e l l s ; T 1 7 c e l l s ; S y n d e c a n - 1 ; I n t e r l e u k i n - 1 7 C O P Y R I G H T T h e A u t h o r ( s ) 2 0 1 8 . P u b l i s h e d b y B a i s h i d e n g P u b l i s h i n g G r o u p I n c . A l l r i g h t s r e s e r v e d . N A M E O F J O U R N A L W o r l d J o u r n a l o f D i a b e t e s I S S N 1 9 4 8-9358PUBLISHERBaishideng Publishing Group Inc, 7901 Stoneridge Drive, Suite 501, Pleasanton, CA 94588, USAWEBSITEHttp://www.wjgnet.com
Name of Journal: World Journal of Diabetes
Manuscript NO: 41940
ManuscriptType: MINIREVIEWS
Unexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17
Jaiswal AK et al. Sdc-1 controls IL17 production
Anil Kumar Jaiswal, Mohanraj Sadasivam, Abdel Rahim A Hamad
Anil Kumar Jaiswal, Department of Pathobiology, Auburn University, Auburn, AL 36849, United States
Mohanraj Sadasivam, Abdel Rahim A Hamad, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, United States
ORCID number: Anil Kumar Jaiswal (0000-0002-8169-0335); Mohanraj Sadasivam ( HYPERLINK "http://orcid.org/0000-0002-3132-2948" \t "_blank" 0000-0002-3132-2948); Abdel Rahim A Hamad (0000-0003-3148-4020).
Author contributions: All authors contributed to conception and writing of this article.
Conflict-of-interest statement: Authors declare no coflict of interest.
Open-Access: This is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Manuscriptsource: Invitedmanuscript
Corresponding author to: Abdel Rahim A Hamad, PhD, Associate Professor, Department of Pathology, School of Medicine, Johns Hopkins University, Ross 66G, 720 Rutland Ave, Baltimore, MD 21205, United States. ahamad@jhmi.edu
Telephone: +1-410-6143021
Fax: +1-410-6143548
Received: September 1, 2018
Peer-review started: September 3, 2018
First decision: October 16, 2018
Revised: October 23, 2018
Acce p t e d : N o v e m b e r 2 6 , 2 0 1 8
A r t i c l e i n p r e s s : N o v e m b e r 2 6 , 2 0 1 8
P u b l i s h e d o n l i n e : D e c e m b e r 1 5 , 2 0 1 8
A b s t r a c t
I n n a t e - l i k e T c e l l s , n a m e l y n a t u r a l k i l l e r T ( N K T ) a n d T c e l l s , p l a y c r i t i c a l r o l e s i n l i n k i n g i n n a t e a n d a d a p t i v e i m m u n e r e s p o n s e s t h r o u g h r a p i d production of cytokines. Prominent among these cytokines is interleukin-17 (IL-17), which is a potent proinflammatory cytokine that plays a critical role in host defense against fungi and extracellular bacteria. However, excessive IL-17-production promotes autoimmune diseases, including psoriasis, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus. IL-17 has also been implicated in regulating body fat, which is highly relevant given rises in obesity and ty p e 2 d i a b e t e s . N K T c e l l s , T c e l l s a n d m u c o s a l - a s s o c i a t e d i n v a r i a n t T c e l l s ( M A I T ) a r e t h e m a j o r s o u r c e s o f I L - 1 7 i n v o l v e d i n p r o t e c t i o n o f m u c o s a l s u r f a c e s f r o m o p p o r t u n i s t i c i n f e c t i o n s a n d c a u s i n g a u t o i m m u n i t y w h e n b e c o m e d y s r e g u l a t e d . G i v e n t h e p a t h o genic effects of IL-17, efforts have been directed towards understanding mechanisms that guard against IL-17 overproduction. One novel potent mechanism is mediated by the heparan sulfate proteoglycan, syndecan-1 (sdc1), which is selectively expressed by IL-17-producing subsets of NKT and T c e l l s . T h i s u n e x p e c t e d r o l e f o r s d c 1 i s u n c o v e r e d b y a n a l y s i s o f N K T a n d T c e l l s i n s d c 1 - d e f i c i e n t m i c e . I n t h i s m i n i - r e v i e w , w e d i s c u s s s e l e c t i v e e x p r e s s i o n o f s d c 1 b y t h e s e i n n a t e T c e l l s a n d c o n s e q u e n c e s o f i t s a b s e n c e o n I L - 1 7 h o m e o s t a s i s a n d p a t h o l o g i c a l i m p l i c a t i o n s .
K e y w o r d s : N a t u r a l k i l l e r T c e l l ; N a t u r a l k i l l e r T 1 7 c e l l s ; T 1 7 c e l l s ; S y n d e c a n - 1 ; I n t e r l e u k i n - 1 7
T h e A u t h o r ( s ) 2 0 1 8 . P u b l i s h e d b y B a i s h i d e n g P u b l i s h i n g G r o u p I n c . A l l r i g h t s r e s e r v e d .
C o r e t i p : I n t e r l e u k i n - 1 7 ( I L - 1 7 ) i s a potent proinflammatory cytokine that plays a critical role in host defense against fungi and extracellular bacteria. Excessive production of IL-17, however, has been implicated in pathogenesis of many autoimmune diseases. Our recent findings show that natural killer T (NKT) cells and T c e l l s e m p l o y s y n d e c a n - 1 ( s d c 1 ) , a h e p a r a n s u l f a t e p r o t e o g l y c a n t h a t i s p r e d o m i n a n t l y e x p r e s s e d b y e p i t h e l i a , t o p r e v e n t o u t o f c o n t r o l e x p a n s i o n o f I L - 1 7 - p r o d u c i n g s u b s e t s o f N K T ( N K T 1 7 ) c e l l a n d ( T 1 7 ) c e l l s . I n t h i s m i n i - r e v i e w , w e h i g h l i g h t t h e se findings and briefly discuss their significance for developing new strategies to prevent IL-17-mediated autoimmme diseases.
Jaiswal AK, Sadasivam M, Hamad ARA. Unexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17. World J Diabetes 2018; In press
INTRODUCTION
Recent data show that innate-like T cells utilize sdc1 to regulate interleukin (IL)-17 production. Significance of this alliance is uncovered by analysis of homeostasis of IL-17 pr o d u c t i o n b y n a t u r a l k i l l e r T ( N K T ) a n d T c e l l s i n s d c 1 - d e f i c i e n t m i c e . T h e r e s u l t s s h o w s i g n i f i c a n t i n c r e a s e s i n s p e c i f i c s u b s e t s o f t h e s e i n n a t e - l i k e T c e l l s t h a t s p e c i a l i z e d i n p r o d u c t i o n o f I L - 1 7 i n t h e t h y m u s a n d i n p e r i p h e r a l o r g a n s i n m i c e l a c k i n g s d c 1 a s i l l u s t r a t e d ( F i g u r e 1 ) . I n t h i s m i n i r e v i e w , w e b r i e f l y d e s c r i b e t h e t h r e e p l a y e r s f o r m i n g t h i s a x i s a n d h o w d e f i c i e n c y o f s d c 1 d y s r e g u l a t e s h o m e o s t a s i s o f I L - 1 7 p r o d u c t i o n b y N K T a n d T c e l l s a n d t h e c o n s e q u e n c e s i n a u t o i m m u n i t y .
S y n d e c a n f a m i ly
The syndecan (sdc) family is comprised of four transmembrane heparan sulfate proteoglycans (HSPGs) ADDIN EN.CITE Bernfield199923232317Bernfield, M.Gotte, M.Park, P. W.Reizes, O.Fitzgerald, M. L.Lincecum, J.Zako, M.Division of Developmental and Newborn Biology, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. bernfield@a1.tch.harvard.eduFunctions of cell surface heparan sulfate proteoglycansAnnu Rev BiochemAnnu Rev Biochem729-7768AnimalsCell Membrane/metabolismHeparan Sulfate Proteoglycans/biosynthesis/*metabolismHumans19990066-4154 (Print)
0066-4154 (Linking)10872465https://www.ncbi.nlm.nih.gov/pubmed/1087246510.1146/annurev.biochem.68.1.729[1]. These four HSPGs are sdc1, 2, 3, and 4. The structures of these sdcs are high conserved with high sequence homology in vertebrates and invertebrates ADDIN EN.CITE ADDIN EN.CITE.DATA [2,3]. Sdc2 is primarily expressed on cells of mesenchymal cells ADDIN EN.CITE ADDIN EN.CITE.DATA [4]; sdc3 is primarily expressed by neuronal tissue and cartilage ADDIN EN.CITE ADDIN EN.CITE.DATA [5], and sdc4 is ubiquitously expressed in most tissues ADDIN EN.CITE ADDIN EN.CITE.DATA [6]. On the other hand, sdc1 is a heparan sulfate that is ubiquitously expressed on epithelial cells, hepatocytes, endothelium. Sdc1 ectodomain interacts with various ligands (including growth factors, chemokines, cytokines and their receptors, and pathogens) to modulate various functions, including differentiation, migration, survival, and proliferation ADDIN EN.CITE Teng201227272717Teng, Y. H.Aquino, R. S.Park, P. W.Department of Medicine, Children's Hospital, Harvard Medical School, Boston, MA 02115, United States.Molecular functions of syndecan-1 in diseaseMatrix BiolMatrix Biol3-16311AnimalsInfection/*metabolism/pathologyInflammation/*metabolism/pathologyMiceMice, KnockoutNeoplasms/*metabolism/pathologySyndecan-1/*genetics/*metabolism2012Jan1569-1802 (Electronic)
0945-053X (Linking)22033227https://www.ncbi.nlm.nih.gov/pubmed/22033227PMC356839410.1016/j.matbio.2011.10.001[7]. It is reported that sdc1 is a target of Blimp-1, the transcription factor that regulates differentiation of B cells into plasma cells. Sdc1 is also involved in the growth and metastasis of multiple myeloma in vivo ADDIN EN.CITE ADDIN EN.CITE.DATA [8]. In contrast, there is very limited information on the role of sdc1 in the adaptive immune cells except as a marker for plasma and myeloma cells and regulators of their survival ADDIN EN.CITE ADDIN EN.CITE.DATA [9,10]. More recently, however, we hav e i d e n t i f i e d s d c 1 a s a m a r k e r o f I L - 1 7 - p r o d u c i n g s u b s e t s o f N K T c e l l s a n d T c e l l s , ( N K T 1 7 a n d T 1 7 ) , r e s p e c t i v e l y . T h e o t h e r m e m b e r s o f s d c s f a m i l y , h o w e v e r , i n t h e r e g u l a t i o n o f c y t o k i n e s i n c l u d i n g I L - 1 7 a r e n o t w e l l d o c u m e n t e d .
I L - 1 7
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