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Mesenchymal Stem Cells from Dental Tissues
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Febe Carolina Vázquez Vázquez, Jael Adrián Vergara-Lope Núñez, Juan José Montesinos, Patricia González-Alva
The interactions between stem cells and the immune system should be mentioned. So far, it has been recognized that MSCs show anti-inflammatory and immune privilege potential, and therefore, they are promising in the treatment of many immune disorders (Huang et al. 2009; Gao et al. 2016).
Retinal stem cell research
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Henry Klassen, Michael J Young, Robert Ritch, Julia E Richards, Teresa Borrάs, Leonard A Levin
The immunologic issues pertaining to brain and retinal transplants are complex and not yet well understood. Sir Peter Medawar, the father of transplantation immunology, realized the scope of the issue himself when he defined the phenomenon of immune privilege. Indeed, until Medawar and his colleagues worked out the principles of transplantation immunology, it was not possible to understand why foreign grafts survived in the anterior chamber but not elsewhere in the body. Medawar understood that the eye and the brain represent special sites where the usual rules of transplantation immunology did not apply. As it turns out, immune privilege results from a number of active regulatory processes rather than immunologic ignorance, as was initially supposed. There is now widespread acceptance of the concept that graft survival is actively promoted by the systemic immune response to cells or tissue placed in immune-privileged sites. It is also known that immune privilege exists in two forms: privileged sites (e.g., eye and brain) and privileged tissues or cells (e.g., testis, cornea, and, as will be discussed, CNS stem cells). The mechanisms responsible for generating and maintaining the privileged status of tissues and sites are similar, but not identical, and may differ from one another.
A look into the testis as a reservoir for HIV and ZIKV—A reproductive biologist’s perspective
Published in C. Yan Cheng, Spermatogenesis, 2018
Elizabeth I. Tang, Christopher L. Robinson, Chi Nok Chong, Shuibing Chen, C. Yan Cheng
Immune privilege is a concept which arose from a group of work that revealed that specific sites in the body, such as the eye, brain, testis, and others, can protect grafted tissue from rejection.1,2 There are two distinct aspects of immune privilege: privileged sites and privileged tissues, which should be noted.3 A privileged site describes a site in which foreign tissue grafts can survive longer, or indefinitely, than in a nonprivileged site. A privileged tissue refers to tissue that resists rejection when grafted into a nonprivileged site. The testis is a unique organ because it encompasses both aspects of immune privilege.4 The first evidence that the testis is immune-privileged dates back to 1786, when John Hunter transplanted a cock testis into the abdomen of a hen.5 This was the first recorded indication that the testis can induce tolerance when transplanted into an allogeneic recipient, as the testis transplant appeared to have no noticeable effects on the hen. During the 1970s, almost 200 years after Hunter’s experiment, evidence that the testis can receive foreign cells and suppress rejection arose. In these studies, tissue allografts or parathyroid glands were implanted in the interstitial space of rat testis and survived.6 These discoveries paved the way for later cotransplantation studies in which pancreatic islet cells were transplanted with testicular Sertoli cells (SCs), which have been found to suppress immune responses, helping the islet cells to survive.7–12 Sertoli cells have been deemed the “nurse” cells of the testis and serve many roles, one of which is conferring immune privilege.
Melanocortin 5 Receptor Expression and Recovery of Ocular Immune Privilege after Uveitis
Published in Ocular Immunology and Inflammation, 2022
Tat Fong Ng, Ambika Manhapra, David Cluckey, Yoona Choe, Srujan Vajram, Andrew W. Taylor
Immune privilege is an evolutionary adaptation that protects the eye from the collateral damage of inflammation to its delicate and non-replicating light-gathering tissues and reduces susceptibility to autoimmune disease. Mice with experimental autoimmune uveitis (EAU), a well-studied rodent model of human endogenous uveitis, enter a stage of chronic retinitis that resolves without therapeutic interventions.32,33 As the untreated EAU mice begin to resolve the retinitis there is an expansion of the suppressor APC in their spleens.8,31 These suppressor APC counter-convert retinal-autoantigen effector T cells into inducible Treg cells, which provide long-term protection from reactivation of autoimmune uveitis.22,30,31 The expansion of the suppressor APC is dependent on the expression of MC5r, and without MC5r expression, there are no detectible retinal-autoantigen specific Treg cells in the spleen post-EAU. When EAU mice are therapeutically treated with α-MSH there is an accelerated resolution of retinitis, and expansion of the suppressor antigen-presenting cells (APC) in the spleen.8,31 Moreover, α-MSH-treated EAU mice have well-preserved retinal structures, and are resistant to re-inducing EAU.18,34
Evaluation of HLA class I and HLA class II allele profile and its relationship with clinical features in patients with alopecia areata: a case–control study
Published in Journal of Dermatological Treatment, 2022
Yıldız Hayran, Melek Gunindi Korkut, Ayşe Öktem, Orhan Şen, Güneş Gür Aksoy, Füsun Özmen
Although the pathogenesis of the disease is not exactly understood, one of the most excepted theories is the breakdown of immune privilege (IP) and T cell-mediated damage of the HF in genetically susceptible patients (8). The concept of IP, first described by Medawar in the 1940s, is accepted as an evolutionary adaptation that provides immune tolerance against foreign antigens and downregulates immune-mediated inflammation for protect certain tissue like pregnant uterus, central nervous system, eyes, testis, and HFs (9). The collapse of IP may lead to immune mediated damage and autoimmune diseases. In HF, physical barriers (absence of lymphatic drainage, extracellular matrix), pro-apoptotic Fas l ligand and programmed cell death 1 ligand (PD-L1) that target immune cells, reduced MICA expression, production of macrophage migration inhibitory factor (MIF), and downregulation of Human Leukocyte Antigen (HLA) expression are the main mechanisms to maintain the IP (10). In HFs of patients with AA, HLA negativity is lost. HLA class I expression is increased and HLA class II molecules are ectopically expressed by keratinocytes of hair bulb suggesting a possible effect of HLA dependent antigen presentation in pathogenesis of AA (8,11,12).
Emerging therapeutic targets for cerebral edema
Published in Expert Opinion on Therapeutic Targets, 2021
Ruchira M. Jha, Sudhanshu P. Raikwar, Sandra Mihaljevic, Amanda M. Casabella, Joshua S. Catapano, Anupama Rani, Shashvat Desai, Volodymyr Gerzanich, J. Marc Simard
The concept of CNS immune privilege has continued to evolve. Previously thought to be devoid of conventional lymphatic vasculature, the role of mLVs in cerebral edema clearance was initially described in 2015 [75,76]. Work in mouse models identified a lymphatic vessel network in the dura matter that absorbs CSF from subarachnoid and interstitial spaces via the glymphatic system [75]. This network ultimately transports this fluid into deep cervical lymph nodes, potentially assisting in the clearance of cerebral edema [75]. Recent zebrafish models suggest that cerebrovascular injury induces rapid ingrowth of mLVs into the injured parenchyma where they become lumenized and drain interstitial fluid (alleviating cerebral edema), and additionally serve as growing tracks for nascent blood vessels [77]. These findings were not corroborated in rodent/primate models: transgenic mice with mLV absence had attenuated clearance of macromolecules and a compromised peripheral immune response, but no difference in brain water content; however, these mice did not have cerebral edema pathology [75,78]. Murine models of glioblastoma multiforme (GBM) and SAH demonstrated impaired lymphatic outflow, increased edema and unfavorable markers of neuroinflammation and apoptosis, suggesting that mLVs. may indeed play a role in both cerebral edema and secondary injury after ABI[72,79,80]. There is emerging evidence that meningeal lymphatic drainage is functionally connected with glymphatic flow.