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The Thymic Defect
Published in Miroslav Holub, Immunology of Nude Mice, 2020
There is, on the other hand, another component of the crude thymosin fraction 5, namely, thymosin beta 4 which is present in a number of tissues including thymus and brain and is synthesized also in mouse peritoneal macrophages;159 high levels of this substance are found in the athymic mouse.159 The authors speculate that thymosin beta 4 may be related to the presence of macrophages in tissues. In respect to these findings, the presence of a “thymic hormone” in spleen, brain, lung, liver, and myocardium159 and not in the dysgenetic thymus appears very unlikely.
Thymus Influence on Differentiation and Functional Maturation of T Lymphocytes
Published in Marek P. Dabrowski, Barbara K. Dabrowska-Bernstein, Immunoregulatory Role of Thymus, 2019
Marek P. Dabrowski, Barbara K. Dabrowska-Bernstein
Although the expression of T lymphocyte surface markers during T cell ontogeny is commonly accepted as a strictly thymic dependent phenomenon, the known specific relations between particular marker and particular thymic factor are surprisingly rare. Even the described property of thymosin beta 4 to induce TdT activity in prothymocytes does not seem to make a good exception. Thymosin beta 4 is synthesized by a variety of tissues in vertebrates, from amphibians to mammals, as a product of a relatively small mRNA resembling that of protamine. High concentrations of thymosin beta 4 have been found in tissues of athymic (nu/nu) mice, indicating not exclusively thymic origin of the peptide. The mechanism of synthesis, wide distribution, and high tissue concentrations of thymosin beta 4 may suggest its role as a physiological structural element of different cells.247 On the other hand, Dalakas et al.,248 using heteroantiserum were able to find thymosin beta 4 in thymic and nonthymic Ia+ cells, including interdigitating cortical and medullary cells, skin Langerhans cells, peritoneal macrophages, and brain oligodendrocytes of man and several other species. The authors hypothesize that all beta 4 positive cells which were found originate from the same bone marrow precursors, express la antigens, and share similar functions of making an ancillary system for T cell reactions at different organs. The word “ancillary” could be perhaps replaced with a little more imaginative expression “complementary” to suggest active participation of both the sides in mutual recognition and immune cooperation.
The Protective Effects of Thymosin-β-4 in a Rat Model of Ischemic Acute Kidney Injury
Published in Journal of Investigative Surgery, 2021
Ugur Aksu, Onur M. Yaman, Ibrahim Guner, Gulcan Guntas, Fuat Sonmez, Gamze Tanriverdi, Mediha Eser, Aris Cakiris, Sibel Akyol, İsmail Seçkin, Hafize Uzun, Nermin Yelmen, Gulderen Sahin
Thymosin-beta-4 (Tβ4) which is mostly produced in the white blood cell, is a small, natural peptide [12] and it was demonstrated that high level of Tβ4 is present to act in the injured area during the repair process [13]. Due to its small size, Tβ4 can readily diffuse into tissues, triggers angiogenesis, and controls the inflammation cascade [14, 15]. Besides suppressing inflammation, Tβ4 modulates endothelial and epithelial cell migration. Hence, Tβ4 could mediate inhibition of tissue swelling and injury [15–17]. In respect of the mechanistic approach, Tβ4 emerges to have an action in modulating inflammation by inhibiting MMPs, blocking tumor necrosis factor (TNF)-α action and activating nuclear factor (NF)-κB [17, 18]. Consistent with the anti-inflammatory effects of Tβ4, its impacts on the cellular level are reflected in a macroscopic level by decreased infarct size [19].
Advances in the Medical Management of Neurotrophic Keratitis
Published in Seminars in Ophthalmology, 2021
Thomas H. Dohlman, Rohan Bir Singh, Reza Dana
Thymosin beta 4 (Tβ4) is a protein that regulates actin polymerization as well as cell differentiation, proliferation and migration, and is expressed by a variety of cells.44 In multiple rodent models of corneal injury, Tβ4 has been shown to promote ocular surface healing by increasing corneal epithelial cell migration, decreasing matrix metalloproteinase expression and decreasing proinflammatory cytokine levels.45–47 The therapeutic potential of Tβ4 in the setting of NK is illustrated by a report describing four patients with chronic non-healing neurotrophic corneal epithelial defects who were treated with Tβ4 four times per day for four weeks.48 In this small case series, three of four patients achieved complete epithelial healing by ten weeks, and the fourth patient had a thin 0.2 × 1.5 mm epithelial defect at the end of follow up. In another small case series, Tβ4 was evaluated in six patients with geographic neurotrophic corneal epithelial defects. Tβ4 was administered four times per day for either four or seven weeks, and patients were followed for an additional 30 days after finishing treatment. Interestingly, at the end of the treatment period, only one patient had achieved complete epithelial healing, while after 30 days of follow up, four of six patients had achieved complete epithelial healing, demonstrating a delayed effect for Tβ4.49
Spotlight on corneal neurotization
Published in Expert Review of Ophthalmology, 2021
Giuseppe Giannaccare, Marco Pellegrini, Federico Bolognesi, Paolo Fogagnolo, Enrico Lupardi, Fabiana Allevi, Federico Bernabei, Alessandro Lozza, Christian Plazza, Claudio Marchetti, Vincenzo Scorcia, Federico Biglioli
Until recently, NK therapy consisted of only supportive measures focused on lubrication and protection of the ocular surface while surgery was limited to refractory cases in order to treat corneal complications. The recent introduction of a recombinant nerve growth factor (Cenegermin, Dompè Farmaceutici, Milan, Italy) has determined a paradigm shift in medical management of NK that previously was only palliative. Although a good efficacy has been showed in clinical trials that reported NK healing in the majority of treated patients, comparisons of corneal sensitivity between treatment group and placebo did not reach statistical significance [8,9]. Furthermore, the high costs still limit its wide diffusion in the routine clinical practice, and as of yet, there are no clinical guidelines on retreatment with Cenegermin in cases of NK recurrence or persistence after the first course of 8 weeks of treatment. Other promising therapies are coming down the pipeline, such as regenerating agent (Cacicol®, OTR3, Paris, France) [59], thymosin beta 4 [60], substance P, and insulin-like growth factor 1 [61], but further studies are needed to validate their safety and efficacy.