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The Host Response to Grafts and Transplantation Immunology
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Acute rejection is the best understood of the three forms of rejection. There is considerable evidence that acute allograft rejection is carried out primarily by T lymphocytes. First, mice that are made deficient in T lymphocytes by neonatal thymectomy, and the so-called “nude” mice that are genetically incapable of making T lymphocytes, fail to reject allografts. In contrast, a deficiency in B lymphocytes does not interfere with allograft rejection. This does not mean that B cells and antibodies are not involved in acute rejection. Rather, their involvement must be dependent on T lymphocytes. Second, it has been shown that T lymphocytes obtained by thoracic duct cannulation of dogs bearing allografts, but not autografts, have the ability to destroy cells derived from the donors of their grafts. This destruction is rapid, efficient, and specific for the graft. The cells which mediate this destruction are the cytolytic T lymphocytes. Since these lymphocytes destroy graft cells in vitro, it has been hypothesized that they destroy grafts in vivo also.
Order Martellivirales: Bromoviridae
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Shahgolzari et al. (2021) used the AMV virions that were isolated and purified from alfalfa Medicago sativa plant as a tool for the in situ vaccination (ISV) against 4T1, an extremely aggressive and metastatic murine triple-negative breast cancer model. The AMV used as an ISV significantly slowed down tumor progression and prolonged survival through immune mechanisms including an increase of costimulatory molecules, inflammatory cytokines, and immune effector cell infiltration and the downregulation of immune-suppressive molecules. It was concluded that the AMV virions appeared to be among the more immunostimulatory plant viruses. Remarkably, they were not cytolytic and did not induce apoptosis of tumor cells directly but rather mediated their impact through stimulating the immune response against the tumor. Therefore, the AMV intratumoral treatment changed the local tumor microenvironment via induction of immune-modulating cytokines and recruitment or phenotypic change of immune cells (Shahgolzari et al. 2021).
An Overview of Drug-Induced Nephropathies *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Jean Paul Fillastre, Michel Godin
Rifampicin is also responsible for many cases of acute interstitial nephritis. The large majority of cases occurred in patients receiving interrupted or discontinuous therapy. High fever with chills, lumbar pains, dark urine, and myalgia are invariably present, rash and eosinophilia rare. Renal failure with or without oliguria supervenes. Hemolysis, thrombopenia, and hepatic cytolysis are sometimes associated. When sought, antirifampicin antibodies detected by an antiglobin test are usually found. Renal biopsy shows an acute monocytic interstitial nephritis without eosinophils. It is to be noted that patients receiving discontinuous treatment have a higher antirifampicin antibody titer than those on continuous therapy. The specific antibodies may persist several months after cessation of therapy. When rifampicin is to be reintroduced after several weeks or months, a search for specific antibodies may be judicious. Almost all patients recover normal renal function, but permanent renal damage has been observed. There is no proof that steroid therapy hastens recovery.
Role of silymarin as antioxidant in clinical management of chronic liver diseases: a narrative review
Published in Annals of Medicine, 2022
Alessio Aghemo, Olga P. Alekseeva, Francesco Angelico, Igor G. Bakulin, Natalia V. Bakulina, Dmitry Bordin, Alexey O. Bueverov, Oxana M. Drapkina, Anton Gillessen, Elvira M. Kagarmanova, Natalia V. Korochanskaya, U. A. Kucheryavii, Leonid B. Lazebnik, Maria A. Livzan, Igor V. Maev, Anatolii I. Martynov, Marina F. Osipenko, Evgenii I. Sas, Antonina Starodubova, Yurii P. Uspensky, Elena V. Vinnitskaya, Emilia P. Yakovenko, Alexey A. Yakovlev
To achieve an antifibrotic effect, silymarin should be used at a dose of 140 mg three times a day for 6–12 months. As per the suggestion of the panel, it is reasonable to use original silymarin as an anti-inflammatory agent along with ursodeoxycholic acid or ademetionine. Additionally, the panel suggested that in patients with inflammation and fibrosis of the liver, original silymarin must be taken for at least 12 months. Silymarin can be used in the complex treatment of patients with viral hepatitis, because as an antioxidant, it reduces toxic load, cytolysis syndrome, and improves the quality of life. Recent progress in treating DILI with original silymarin is very encouraging. For managing ALD, alcohol needs to be eliminated before contemplating hepatoprotection with silymarin. There is a clear clinical rationale for using an antioxidant such as silymarin as a hepatoprotective and hepatotropic agent. Further, silymarin treatment may begin early and may be prolonged with careful monitoring of liver enzymes. The expert panel opined that original silymarin would have a clear advantage over other marketed generic formulations in terms of its high concentration, bioavailability, safety, effectiveness, and quality. Further, a large body of scientific evidence built on original silymarin studies can be leveraged in this regard. The panel also opined that as original silymarin is a safe and effective drug and as there exists an evidence base on its clinical and biochemical effects, it can be recommended for the treatment of CLDs.
Nivolumab and anti-HCV activity, a case report
Published in Acta Clinica Belgica, 2021
Laura Wuyts, Annelies Janssens, Luisa Vonghia, Peter Michielsen, Jo Raskin, Ann Driessen, Stijn Van Hees, Sven Francque, Thomas Vanwolleghem
Activation of the immune system by immune checkpoint inhibitors may also lead to immune responses directed at normal tissue and consequently induce autoimmune adverse events. These most commonly affect the skin (rash, xerosis, pruritus), the gastrointestinal tract (colitis, diarrhea), the liver (hepatitis), and endocrine organs (hypophysitis, thyroiditis). Any organ may be affected [1]. On the other hand, data from prospective studies suggest that the safety profile of nivolumab is manageable in chronically HCV-infected patients [2,4]. In phase I–II studies of nivolumab for HCC, a total of 262 patients were included, of which 48 in a dose-escalation phase (0.1–10 mg/kg/2 weeks) and 24 in a dose-expansion phase (3 mg/kg/2 weeks). Three (6%) patients had treatment-related serious adverse events, two of which a grade ≥3 hepatitis, as described by the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE): cytolysis and/or cholestasis more than 5 times, bilirubin more than 3 times upper limit of normal (ULN) [2,4]. In a phase III study with pembrolizumab, a humanized IgG4 kappa monoclonal anti-PD1 antibody, a grade 3/4 hepatoxicity was seen in 4% of patients [7].
TCR repertoire characteristics predict clinical response to adoptive CTL therapy against nasopharyngeal carcinoma
Published in OncoImmunology, 2021
Guoping Wang, Poorva Mudgal, Liuyang Wang, Timothy Wai Ho Shuen, Haiyang Wu, Peter B Alexander, Who-Whong Wang, Ying Wan, Han Chong Toh, Xiao-Fan Wang, Qi-Jing Li
For EBV-CTL therapy, or any other T cell-mediated immunotherapies, efficacy is determined by both the efficiency of tumor antigen presentation and in situ T cell activation.4 On the antigen presentation side, tumors heavily loaded with homogeneously distributed immunogenic antigens are most susceptible to T cell-mediated killing.4,5 High human leukocyte antigen (HLA) expression supports a higher probability of tumor antigen presentation to reduce the chance of immune evasion.5 On the T cell activation side, the tumor microenvironment plays a pivotal role by restricting the capacity of T cell proliferation and cytolytic function.4 Besides these extrinsic factors, intrinsic T cell activation, proliferation, and cytokine secretion are controlled by a T cell’s differentiation state,4,6 and most importantly, its antigen binding structure, the T cell receptor (TCR).7,8