Pio Conti1, Alessandro Caraffa2, Gianpaolo Ronconi3, Spiros K Kritas4, Filiberto Mastrangelo5, Lucia Tettamanti6, Ilias Frydas7, Theoharis C Theoharides8. 1. Immunology Division, Postgraduate Medical School, University of Chieti-Pescara, Chieti, Italy. pconti@unich.it. 2. Department of Pharmacy, University of Perugia, Perugia, Italy. 3. Clinica dei Pazienti del Territorio, Policlinico Gemelli, Rome, Italy. 4. Department of Microbiology, University of Thessaloniki, Thessaloniki, Greece. 5. Department of Medical Science and Biotechnology, University of Foggia, Foggia, Italy. 6. Department of Medical and Morphological Science, University of Insubria, Varese, Italy. 7. Department of Parasitology Veterinary School, Aristotelian University, Thessaloniki, Greece. 8. Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA, USA.
Abstract
OBJECTIVE: The aim of this study was to evaluate the role of mast cells (MCs) in allograft rejection, eventually inhibited by IL-37. Immune cells including MCs participate in allograft rejection by generating IL-1, IL-33, TNF and other cytokines. METHODS: We evaluated allograft rejection on the experience of our experimental data and using the relevant literature. RESULTS: MCs are involved in initiation and regulation of innate and adaptive immune responses-pathways. MCs are important pro-inflammatory cells which express high-affinity receptor FceRI and can be activated by IgE and some pro-inflammatory cytokines, such as IL-1 and IL-33. The cross-linkage of high affinity IgE receptor on MCs by antigen ligation has a crucial role in allergy, asthma, anaphylaxis, cancer and allograft rejection. MCs mediate immunity in organ transplant, leading to the activation of allospecific T cells implicated in the rejection and generate pro-inflammatory cytokines/chemokines. IL-1 pro-inflammatory cytokine family members released by MCs mediate allograft rejection and inflammation. IL-37 is also an IL-1 family member generated by macrophage cell line in small amounts, which binds to IL-18Rα and produces an anti-inflammatory effect. IL-37 provokes the inhibition of TLR signaling, TLR-induced mTOR and (MyD88)-mediated responses, suppressing pro-inflammatory IL-1 family members and increasing IL-10. CONCLUSION: IL-37 inhibition offers the opportunity to immunologically modulate MCs, by suppressing their production of IL-1 family members and reducing the risk of allograft rejection, resulting as a potential good therapeutic new cytokine. Here, we report the relationship between inflammatory MCs, allograft rejection and pro-inflammatory and anti-inflammatory IL-37.
OBJECTIVE: The aim of this study was to evaluate the role of mast cells (MCs) in allograft rejection, eventually inhibited by IL-37. Immune cells including MCs participate in allograft rejection by generating IL-1, IL-33, TNF and other cytokines. METHODS: We evaluated allograft rejection on the experience of our experimental data and using the relevant literature. RESULTS: MCs are involved in initiation and regulation of innate and adaptive immune responses-pathways. MCs are important pro-inflammatory cells which express high-affinity receptor FceRI and can be activated by IgE and some pro-inflammatory cytokines, such as IL-1 and IL-33. The cross-linkage of high affinity IgE receptor on MCs by antigen ligation has a crucial role in allergy, asthma, anaphylaxis, cancer and allograft rejection. MCs mediate immunity in organ transplant, leading to the activation of allospecific T cells implicated in the rejection and generate pro-inflammatory cytokines/chemokines. IL-1 pro-inflammatory cytokine family members released by MCs mediate allograft rejection and inflammation. IL-37 is also an IL-1 family member generated by macrophage cell line in small amounts, which binds to IL-18Rα and produces an anti-inflammatory effect. IL-37 provokes the inhibition of TLR signaling, TLR-induced mTOR and (MyD88)-mediated responses, suppressing pro-inflammatory IL-1 family members and increasing IL-10. CONCLUSION:IL-37 inhibition offers the opportunity to immunologically modulate MCs, by suppressing their production of IL-1 family members and reducing the risk of allograft rejection, resulting as a potential good therapeutic new cytokine. Here, we report the relationship between inflammatory MCs, allograft rejection and pro-inflammatory and anti-inflammatory IL-37.
Authors: Jama Jahanyar; Michael M Koerner; Matthias Loebe; Keith A Youker; Guillermo Torre-Amione; George P Noon Journal: Transplantation Date: 2008-05-27 Impact factor: 4.939
Authors: Charlotte E M de Mooij; Mihai G Netea; Walter J F M van der Velden; Nicole M A Blijlevens Journal: Blood Date: 2017-05-08 Impact factor: 22.113
Authors: Alexandra Taracanova; Mihail Alevizos; Anna Karagkouni; Zuiy Weng; Errol Norwitz; Pio Conti; Susan E Leeman; Theoharis C Theoharides Journal: Proc Natl Acad Sci U S A Date: 2017-05-01 Impact factor: 11.205
Authors: P Conti; Al Caraffa; S K Kritas; G Ronconi; G Lessiani; E Toniato; T C Theoharides Journal: J Biol Regul Homeost Agents Date: 2017 Apr-Jun Impact factor: 1.711
Authors: Pio Conti; Luisa Stellin; Alesssandro Caraffa; Carla E Gallenga; Rhiannon Ross; Spyros K Kritas; Ilias Frydas; Ali Younes; Paolo Di Emidio; Gianpaolo Ronconi Journal: Int J Mol Sci Date: 2020-06-16 Impact factor: 5.923