Dr. Dipyaman Ganguly
Ramanujan Fellow, Department of Science & Technology, Govt. of India
2017: NASI-Scopus Young Scientist Award in Medicine
2013-2018: Ramanujan Fellow, SERB, Department of Science & Technology, India
2010-2012: S.L.E. Foundation Postdoctoral Fellow, College of Physicians & Surgeons, Columbia University Medical Center, New York City, USA.
2006-2010: PhD (Immunology & Biomedical Sciences), University of Texas MD Anderson Cancer Center, Houston, USA.
2003-2006: PhD (Biotechnology), Indian Institute of Chemical Biology, Kolkata, India.
1996-2002: MBBS (Medical College & Hospitals, Calcutta), Calcutta University, Kolkata, India.
The basic premise for immune algorithm is distinguishing self from nonself. This is achieved by different modules of host immune system. The ‘innate’ immune system recognizes the nonself based on predominantly nonself-associated molecular patterns (PAMPs), while the ‘adaptive’ immune axis adapts to the nonself molecular determinants. These two work together toward an effective immune response. An effective immune response to an invading pathogen (nonself) leads to protective immunity and a defective response leads to overt infection. On the other hand, an unintended response to the self-entities leads to autoimmune disorders, while a misjudged tolerance to the altered self contributes to tumorigenesis. Our research broadly concentrates on role of innate immune axis in the crossroads of infection, autoimmunity and cancer. Dendritic cells (DCs) are the innate cells with most of the decision-making responsibilities for an ensuing immune response or tolerance. We try to decipher the governing principles of self-nonself discrimination by the germline-encoded invariant pattern recognition receptors (PRRs) expressed by DCs and how they work in a given clinical context. Broadly the research directions of our lab are:
- Innate immune regulation and molecular mechanisms of dendritic cell function
- Role of innate immune deregulation in autoreactive inflammation
- Deciphering the role and modulation of dendritic cells in tumor microenvironment and cancer immunotherapy
- Neuro-immune interface: physico-biochemical crosstalk between the central nervous system and the innate immune system r
Ours is a very new laboratory in IICB that promises a lot of fun and exciting science, which will be achieved through hard work of all its members. Feel free to contact Dipyaman if you feel like sharing the excitement.
- Roopkatha Bhattacharya, M.Sc., CSIR-JRF, Email: firstname.lastname@example.org
- Oindrila Rahaman, M.Sc.,UGC-JRF,Email: email@example.com
- Deblina Raychaudhuri, M.Sc.,CSIR Shyama Prasad Mukherjee Fellow (JRF); Email: firstname.lastname@example.org
- Dr. Shamik Bhattacharya, M.Sc., Ph.D.,Postdoctoral Research Associate (DBT),Email: email@example.com
- Dr. Pritam Duttagupta, MBBS,Visiting Fellow,Email: firstname.lastname@example.org
- Chinky Shiu Chen Liu,M.Sc .,CSIR-JRF,Email: email@example.com
At this point of time our laboratory cannot accommodate any more fellows. But from time to time we look for individuals with excellent academic credentials and predoctoral [NET (CSIR/UGC] or postdoctoral fellowships — candidates with some background in human physiology, or immunology with exposure to molecular biology techniques are preferred. Medical graduates/postgraduates (MBBS/MD) interested in biomedical research should also feel free to discuss possibilities of joining the team. Interested candidates may contact directly at firstname.lastname@example.org along with curriculum vita and a brief statement on research interests.
- Nargis T, Kumar K, Ghosh AR, Sharma A, Rudra D, Sen D, Chakrabarti S, Mukhopadhyay S, Ganguly D#, Chakrabarti P# (#Corresponding authors). KLK5 induces shedding of DPP4 from circulatory Th17 cells in type 2 diabetes. Molecular Metabolism. 2017 Nov;6(11):1529-1539. (In media: http://www.business-standard.com/article/news-ians/scientists-stumble-upon-potential-drug-target-for-diabetes-117102500537_1.html )
- Ganguly D. Do type I interferons link systemic autoimmunities and metabolic syndrome in a pathogenetic continuum? Trends in Immunology. 2017 Aug 17. [Epub ahead of print]
- Roy S, Mukherjee A, Paul B, Rahaman O, Roy S, Maithri G, Ramya B, Pal S, Ganguly D#, Talukdar A# (#Corresponding authors). Design and Development of benzoxazole derivatives with toll-like receptor 9 antagonism. European Journal of Medicinal Chemistry. 2017. 134:334-347.
- Ghosh AR, Bhattacharya R, Bhattacharya S, Nargis T, Rahaman O, Duttagupta P, Raychaudhuri D, Chen Liu CS, Roy S, Ghosh P, Khanna S, Chaudhuri T, Tantia O, Haak S, Bandyopadhyay S, Mukhopadhyay S, Chakrabarti P, Ganguly D. Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation. Diabetes. 2016. 65 (11): 3440-3452.
(In media: http://indianexpress.com/article/lifestyle/health/why-the-obese-are-prone-to-diabetes-a-protein-gives-a-clue/; http://www.ndtv.com/health/indian-scientists-discover-link-between-obesity-diabetes-1455710 ; http://www.hindustantimes.com/health-and-fitness/why-does-obesity-cause-diabetes-indian-scientists-just-found-an-explanation/story-M2ExSvGoD4DjjSodszeVrL.html ; http://www.anandabazar.com/lifestyle/do-we-get-diabetic-with-the-increase-of-fat-1.476272# ; https://www.telegraphindia.com/1160908/jsp/nation/story_107007.jsp#.WN9XljuGPIW )
- Meller S, Di Domizio J, Voo KS, Friedrich HC, Chamilos G, Ganguly D, Conrad C, Gregorio J, Le Roy D, Roger T, Ladbury JE, Homey B, Watowich S, Modlin RL, Kontoyiannis DP, Liu YJ, Arold ST, Gilliet M. T helper 17 cells promote microbial killing and innate immune sensing of DNA via interleukin-26. Nature Immunology. 2015 Sep;16(9):970-9.
- Lande R*, Chamilos G*, Ganguly D*, Demaria O, Frasca L, Durr S, Conrad C, Schröder J, Gilliet M (*equal contribution). Cationic antimicrobial peptides in psoriatic skin cooperate to break innate tolerance to self-DNA. European Journal of Immunology. 2015 Jan;45(1):203-13.
- Sisirak V*, Ganguly D*, Lewis KL, Couillault C, Tanaka L, Bolland S, D’Agati V, Elkone KB, Reizis B (*equal contribution). Genetic evidence for the role of plasmacytoid dendritic cells in systemic lupus erythematosus. Journal of Experimental Medicine. 2014 Sep 22;211(10):1969-76.
- Ganguly D, Haak S, Sisirak V, Reizis B. Role of dendritic cells in autoimmunity. Nature Reviews Immunology. 2013 Aug;13(8):566-77.
- Di Domizio J, Dorta-Estremera S, Gagea M, Ganguly D, Meller S, Li P, Zhao B, Tan FK, Bi L, Gilliet M, Cao W. Nucleic acid-containing amyloid fibrils potently induce type I interferon and stimulate systemic autoimmunity. Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14550-5.
- Lande R, Ganguly D, Facchinetti V, Frasca L, Conrad C, Gregorio J, Meller S, Chamilos G, Sebasigari R, Riccieri V, Bassett R, Amuro H, Fukuhara S, Ito T, Liu YJ, Gilliet M. Neutrophils activate plasmacytoid dendritic cells by releasing self-DNA-peptide complexes in systemic lupus erythematosus. Science Translational Medicine. 2011 Mar 9;3(73):73ra19. doi: 10.1126/scitranslmed.3001180. Commentary in New England Journal of Medicine, 2011, 365(8):758-60; featured in Nature Reviews Key Advances in Medicine, 2012.
- Ganguly D, Chamilos G, Lande R, Gregorio J, Meller S, Facchinetti V, Homey B, Barrat FJ, Zal T, Gilliet M. Self-RNA-antimicrobial peptide complexes activate human dendritic cells through TLR7 and TLR8. Journal of Experimental Medicine. 2009 Aug 31;206(9):1983-94. Recommended by Faculty1000 with FFa factor of 12.
- Chamilos G, Ganguly D, Lande R, Gregorio J, Meller S, Goldman WE, Gilliet M, Kontoyiannis DP. Generation of IL-23 producing dendritic cells (DCs) by airborne fungi regulates fungal pathogenicity via the induction of T(H)-17 responses. PLoS One. 2010 Sep 23;5(9):e12955.
- Ganguly D, Paul K, Bagchi J, Rakshit S, Mandal L, Bandyopadhyay G, Bandyopadhyay S. Granulocyte-macrophage colony-stimulating factor drives monocytes to CD14low CD83+ DCSIGN- interleukin-10-producing myeloid cells with differential effects on T-cell subsets. Immunology. 2007 Aug;121(4):499-507.
- Ghosh M, Mandal L, Maitra S, Rakshit S, Paul K, Bagchi J, Ganguly D, Pal C, Bandyopadhyay S. Leishmania donovani infection of human myeloid dendritic cells leads to a Th1 response in CD4+ T cells from healthy donors and patients with Kala-azar. Journal of Infectious Disease. 2006 Aug 1;194(3):294-301.