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General Thermography
Published in James Stewart Campbell, M. Nathaniel Mead, Human Medical Thermography, 2023
James Stewart Campbell, M. Nathaniel Mead
The thymus gland is located in the anterior chest, in front of the upper portion of the heart and trachea (Figure 10.61). It is proportionally large in infancy but shrinks with age. At puberty, it weighs 30 to 50 grams, and by old age, it typically weighs 5 to 15 grams. The thymus rarely becomes neoplastic, developing into a lymphoma or thymoma. Lymphomas occupying superficial lymph nodes may appear warm on thermographic analysis, but this warmth is not associated with the thymus gland itself.165 Thymomas, on the other hand, may become large enough to become detectable as a warm area in the upper anterior chest, but no studies confirming this have been published. Though some thermographers claim that cool areas over the anterior or posterior upper chest are a sign of “underactive thymus,” this is doubtful because of the small size and normally low metabolic activity of the gland in adulthood. A cool area over the upper sternum may instead be due to the presence of thymic cysts, which may become as large as 4 cm (1.6 in.) in diameter. No studies are available concerning cool areas over the thymus gland. MRI and CAT scans can determine anatomic thymus abnormalities, while hematology can monitor the physiologic and pathologic activity of the gland.166
The immune and lymphatic systems, infection and sepsis
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Michelle Treacy, Caroline Smales, Helen Dutton
T cells are produced by the red bone marrow and matured in the thymus gland. The four main types of differentiated T cell are: T helper inducer T cells (T4).Cytotoxic T cells (T8).Memory T cells.
Inflammation and the Immune System
Published in Jeremy R. Jass, Understanding Pathology, 2020
The separation of lymphocytes into T cells and B cells began through investigations of the thymus gland. Up until the 1960s the thymus gland was usually classed as an endocrine gland, yet its removal in both animals and humans (due to thymic cancer, for example) has no appreciable effect. The thymus is large in newborn humans and other newborn mammals, reaches its maximum size at around puberty (though by then has become relatively small compared with other organs), and then undergoes progressive atrophy.
Growth hormone enhances the CD34+ stem cells repopulation of the male albino rat thymus gland in cyclophosphamide induced injury: immunohistochemical and electron microscopic study
Published in Ultrastructural Pathology, 2023
Amira I. Shrief, Walaa H.E. Hamed, Shireen A Mazroa, Amal M. Moustafa
Examination of the sections in the thymus gland of all subgroups of control rats (group І) revealed the same structure. The thymus gland was covered with a thin connective tissue capsule and was subdivided into intercommunicating lobules by thin connective tissue septa. Each lobule was divided into outer darkly stained cortex and inner pale medulla with a clear demarcation between them (Figure 1a). The thymic cortex was populated mainly by large number of closely packed thymoblasts and fewer epithelial reticular cells (ERCs). Thymoblasts had large rounded nuclei. The ERCs had oval to round pale stained nuclei. Macrophages and blood capillaries were also seen (Figure 1b). The thymic medulla was formed of loosely packed thymocytes with small rounded deeply stained nuclei, more prominent ERCs and few Hassall’s corpuscles. Hassall’s corpuscles were formed of a central hyaline acidophilic mass surrounded with one layer of ERCs (Figure 1c).
An update on the use of immunoglobulins as treatment for myasthenia gravis
Published in Expert Review of Clinical Immunology, 2022
Monica Alcantara, Carolina Barnett, Hans Katzberg, Vera Bril
Myasthenia gravis (MG) is an autoimmune neuromuscular disease where pathogenic antibodies are directed against the skeletal muscle nicotinic acetylcholine receptor (AChRab), and less commonly to other proteins at the post-synaptic neuromuscular junction such as the muscle-specific kinase (MuSK) and low-density lipoprotein receptor-related protein 4 (LRP4) [1]. Being an antibody-mediated disease where the main mechanisms are related to T-cell activation and interactions with CD4 + T and B cells, immunosuppressive and immunomodulating medications are the cornerstone therapy to counteract the disruption of the immune system and to suppress autoreactive cells. The thymus gland is central to the pathophysiology of AChRab-mediated MG, and surgical treatment with thymectomy is warranted in AchR-Ab+ adult patients (particularly those 18–50 years-old, although it may be recommended to patients up to 65 years old) and in those with thymoma [2–5].
Role of IL-17 in asthma pathogenesis and its implications for the clinic
Published in Expert Review of Respiratory Medicine, 2019
Rakhee K Ramakrishnan, Saba Al Heialy, Qutayba Hamid
Naïve CD4+ T cells developing in the thymus gland are activated by stimulatory signals which direct their differentiation into multiple lineages of effector T cells. The integration of three proximal signals direct the differentiation of naïve T cells to Th17 cells. Naïve T cell differentiation is initiated upon engaging both the T cell receptor (Signal 1) and costimulatory molecules (Signal 2). However, lineage commitment to a particular subset of T-helper cell is directed by cytokines secreted by the innate immune cells (Signal 3). The differentiation of Th17 cells is dependent on the lineage-specific transcription factor, retinoic acid receptor-related orphan receptor-γt (ROR-γt), and involves the coordinated activities of both pro-inflammatory and anti-inflammatory cytokines [11,12]. The development of Th17 cells is completed in three stages: induction of differentiation in the presence of TGF-β together with IL-6, amplification of Th17 response requires the action of IL-21 in an autocrine loop and stabilization of the IL-17 phenotype requires IL-23 [12]. It is striking that TGF-β alone induces the Treg-specific transcription factor FOXP3, however, in combination with IL-6 induces the expression of ROR-γt that is selectively expressed in Th17 cells.