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Stefania Gallucci, MD
Associate Professor, Microbiology and Immunology
Associate Professor, Temple Autoimmunity Center
Department of Microbiology and Immunology
Temple Autoimmunity Center
MD, Universita’ Cattolica del Sacro Cuore (UCSC), Rome, Italy, 1992
Residency, Clinical Pathology and Laboratory Medicine, Universita’ Cattolica del Sacro Cuore (UCSC), Rome, Italy, 1992-1996
Fellowship, Visiting Fellow in Immunology, NIAID, NIH, Bethesda, MD, USA, 1996-1999
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- Biology of dendritic cells: Dendritic cell activation and Endogenous Danger Signals (i.e. Type I Interferons)
- Effects of apoptotic/necrotic cells on dendritic cell functions
- Role of dendritic cells in lupus pathogenesis
The main interest of the laboratory is the initiation and regulation of the immune response. In particular, we study dendritic cells (DCs), the most important antigen-presenting cells and pivotal stimulators of the immune response as well as the induction of immunological tolerance. Our goals are to understand how dendritic cells activate and test in animal models novel factors able to modulate DC function and, therefore, regulate the immune response.
Dendritic cell activation. Our long-term goal is to discover biologic factors able to activate the function of dendritic cells in order to improve DC-based and other innovative vaccines needed to fight tumors and infectious diseases.
Danger Signals. DCs reside in the different tissues and organs of our body in a resting state and monitor the environment for Danger Signals, stimuli able to activate DCs. Danger Signals can be endogenous, derived from tissues undergoing stress, damage or non-physiologic cell death, or can be exogenous, derived from pathogens. Weak vaccines require the addition of effective adjuvants to improve their immunogenicity and investigating Endogenous Danger signals can suggest novel adjuvants to be used in vaccine development. We are studying the Type I Interferons (IFNs), a family of endogenous Danger Signals involved in the activation of DCs and in the regulation of the immune response. Through the investigation of the signaling pathways triggered downstream of the Type I Interferon Receptor (IFNAR), we aim to discover ways to augment but also to inhibit the response of the immune cells to Type I IFNs.
Induction of Tolerance. Our long-term goal is to discover biologic factors able to induce a stable tolerogenic function in dendritic cells that can be used in immunotherapy of conditions, such as transplantation and autoimmunity, in which excessive and inappropriate immune responses are causing morbidity and mortality.
Autoimmunity. We investigate the role of DCs in the pathogenesis of the autoimmune disease Systemic Lupus Erythematosus. We study spontaneous and induced models of murine lupus to determine how the DCs affect the autoimmune process; we have found that DC costimulatory and cytokine profile, APC activity and life span are altered and we are focusing our efforts on the role of Type I IFNs in such abnormalities. Using techniques of traditional cellular immunology and cutting edge molecular biology, we are studying cytokines, such as IL-4, that can suppress the response of DCs to Type I IFNs, and we are testing in vivo novel therapeutic approaches to ameliorate the severity and ultimately to cure the autoimmune disease. In addition, we are developing novel protocols of gene transfer specifically targeting Antigen Presenting Cells. If successful, these approaches will be invaluable for delivery of genes for immune-modulation and induction of tolerance in autoimmunity as well as in transplantation.
Transplantation. We have recently discovered that Complement Receptor 3, a surface receptor that can bind opsonized apoptotic cells, suppresses DC immunogenicity. We are investigating whether CR3 can be exploited to induce immune tolerance in solid organ tranplantation. Our fundamental goal is to generate therapeutic protocols in rodents that can quickly and directly be applied first to larger animals and eventually to transplantation patients, in combination with the present immunosuppressive regime and, ultimately, in novel tolerogenic regimes.
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Recent Medically Related Publications, Obtained from PubMed (Click on PubMed ID to view abstract)
22661089. Sriram U, Varghese L, Bennett HL, Jog NR, Shivers DK, Ning Y, Behrens EM, Caricchio R, Gallucci S, Myeloid dendritic cells from B6.NZM Sle1/Sle2/Sle3 lupus-prone mice express an IFN signature that precedes disease onset. J Immunol 189:1(80-91)2012 Jul 1
22031761. Huang Y, Biswas C, Klos Dehring DA, Sriram U, Williamson EK, Li S, Clarke F, Gallucci S, Argon Y, Burkhardt JK, The actin regulatory protein HS1 is required for antigen uptake and presentation by dendritic cells. J Immunol 187:11(5952-63)2011 Dec 1
19454727. Jog NR, Dinnall JA, Gallucci S, Madaio MP, Caricchio R, Poly(ADP-ribose) polymerase-1 regulates the progression of autoimmune nephritis in males by inducing necrotic cell death and modulating inflammation. J Immunol 182:11(7297-306)2009 Jun 1
18713972. Behrens EM, Ning Y, Muvarak N, Zoltick PW, Flake AW, Gallucci S, Apoptotic cell-mediated immunoregulation of dendritic cells does not require iC3b opsonization. J Immunol 181:5(3018-26)2008 Sep 1
17982033. Sriram U, Biswas C, Behrens EM, Dinnall JA, Shivers DK, Monestier M, Argon Y, Gallucci S, IL-4 suppresses dendritic cell response to type I interferons. J Immunol 179:10(6446-55)2007 Nov 15
17475855. Behrens EM, Sriram U, Shivers DK, Gallucci M, Ma Z, Finkel TH, Gallucci S, Complement receptor 3 ligation of dendritic cells suppresses their stimulatory capacity. J Immunol 178:10(6268-79)2007 May 15
16772370. Biswas C, Sriram U, Ciric B, Ostrovsky O, Gallucci S, Argon Y, The N-terminal fragment of GRP94 is sufficient for peptide presentation via professional antigen-presenting cells. Int Immunol 18:7(1147-57)2006 Jul
16507174. Colonna L, Dinnall JA, Shivers DK, Frisoni L, Caricchio R, Gallucci S, Abnormal costimulatory phenotype and function of dendritic cells before and after the onset of severe murine lupus. Arthritis Res Ther 8:2(R49)2006
16237113. Zheng Y, Gallucci S, Gaughan JP, Gross JA, Monestier M, A role for B cell-activating factor of the TNF family in chemically induced autoimmunity. J Immunol 175:9(6163-8)2005 Nov 1
16081846. Frisoni L, McPhie L, Colonna L, Sriram U, Monestier M, Gallucci S, Caricchio R, Nuclear autoantigen translocation and autoantibody opsonization lead to increased dendritic cell phagocytosis and presentation of nuclear antigens: a novel pathogenic pathway for autoimmunity? J Immunol 175:4(2692-701)2005 Aug 15
11238605. Anderson CC, Carroll JM, Gallucci S, Ridge JP, Cheever AW, Matzinger P, Testing time-, ignorance-, and danger-based models of tolerance. J Immunol 166:6(3663-71)2001 Mar 15
11154927. Gallucci S, Matzinger P, Danger signals: SOS to the immune system. Curr Opin Immunol 13:1(114-9)2001 Feb
10545990. Gallucci S, Lolkema M, Matzinger P, Natural adjuvants: endogenous activators of dendritic cells. Nat Med 5:11(1249-55)1999 Nov
9576614. Gallucci S, Provenzano C, Mazzarelli P, Scuderi F, Bartoccioni E, Myoblasts produce IL-6 in response to inflammatory stimuli. Int Immunol 10:3(267-73)1998 Mar
7507012. Bartoccioni E, Gallucci S, Scuderi F, Ricci E, Servidei S, Broccolini A, Tonali P, MHC class I, MHC class II and intercellular adhesion molecule-1 (ICAM-1) expression in inflammatory myopathies. Clin Exp Immunol 95:1(166-72)1994 Jan
1472645. Bartoccioni E, Gallucci S, Evoli A, Scuderi F, Thymulin and ocular myasthenia gravis. Autoimmunity 13:4(337-8)1992
3359643. Carlomagno G, Benussi G, Candussi G, Gallucci S, A simple local database for audit and epidemiologic studies. Clin Exp Obstet Gynecol 15:1-2(31-3)1988
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Uma Sriram, PhD
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