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Pathology and genetics of tumours of the lung , pleura, thymus and heart

Recent elucidation of the role of central tolerance in preventing organ-specific autoimmunity has changed our concepts of self/nonself discrimination. This paradigmatic shift is largely attributable to the discovery of promiscuous expression of tissue-restricted self-antigens (TRAs) by medullary thymic epithelial cells (mTECs). TRA expression in mTECs mirrors virtually all tissues of the body, irrespective of developmental or spatio-temporal expression patterns. This review summarizes current knowledge on the cellular and molecular regulation of TRA expression in mTECs, outlines relevant mechanisms of antigen presentation and modes of tolerance induction, and discusses implications for the pathogenesis of autoimmune diseases and other biological processes such as fertility, pregnancy, puberty, and tumor defense.

A central role for central tolerance

Background Adult Burkitt-type lymphoma (BL) and acute lymphoblastic leukemia (B-ALL) are rare entities composing 1% to 5% of non-Hodgkin lymphomas NHL) or ALL. Prognosis of BL and B-ALL has been poor with conventional NHL or ALL regimens, but has improved with dose-intensive regimens. Methods To evaluate the addition of rituximab, a CD20 monoclonal antibody, to intensive chemotherapy in adults with BL or B-ALL, 31 patients with newly diagnosed BL or B-ALL received the hyper-fractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (hyper-CVAD) regimen with rituximab. Their median age was 46 years; 29% were 60 years or older. Rituximab 375 mg/m(2) was given on Days 1 and 11 of hyper-CVAD courses and on Days 1 and 8 of methotrexate and cytarabine courses. Results Complete remission (complete response [CR]) was achieved in 24 of 28 (86%) evaluable patients; 3 had a partial response, and 1 had resistant disease. There were no induction deaths. The 3-year overall survival (OS), event-free survival, and disease-free survival rates were 89%, 80%, and 88%, respectively. Nine elderly patients achieved CR with all of them in continuous CR (except 1 death in CR from infection), with a 3-year OS rate of 89%. Multivariate analysis of current and historical (those treated with hyper-CVAD alone) groups identified age and treatment with rituximab as favorable factors. Conclusions The addition of rituximab to hyper-CVAD may improve outcome in adult BL or B-ALL, particularly in elderly patients.

/pdf/chemoimmunotherapy-with-hyper-cvad-plus-rituximab-for-the-2yme9haeto.pdf

Chemoimmunotherapy with hyper-CVAD plus rituximab for the treatment of adult Burkitt and Burkitt-type lymphoma or acute lymphoblastic leukemia

Myasthenia gravis is a relatively rare neurological disease that is associated with loss of the acetylcholine receptors that initiate muscle contraction. This results in muscle weakness, which can be life-threatening. The story of how both the physiological basis of the disease and the role of acetylcholine-receptor-specific antibodies were determined is a classic example of the application of basic science to clinical medicine, and it has provided a model for defining other antibody-mediated disorders of the peripheral and central nervous systems.

Unravelling the pathogenesis of myasthenia gravis.

AML with 11q23/MLL abnormalities as defined by the WHO classification: incidence, partner chromosomes, FAB subtype, age distribution, and prognostic impact in an unselected series of 1897 cytogenetically analyzed AML cases

Myasthenia gravis (MG) is an autoimmune disease caused by autoantibodies against the acetylcholine receptor (AChR) at the neuromuscular junction [1]. The muscular AChR has been extensively characterized [2], but whether the muscular AChR plays a role during the initiation of MG is unknown [3]. The muscular AChR is a pentameric ion channel composed of 4 different subunits [2, 4]. The fetal AChR expressed during intrauterine life and after denervation of adult muscle exhibits an α2βδγ composition, while the adult AChR expressed after birth in innervated muscle exhibits an α2βδγ composition [4]. The α-subunit contains the main epitopes recognized by MG autoantibodies [2]. The human muscle AChR α-subunit exists as two isoforms, P3A- and P3A+ [5]. The P3A+ isoform does not bind α-bungarotoxin or monoclonal antibodies against the AChR main immunogenic region and is not integrated into functional AChR [6]. Studies on the expression of the various AChR subunits in thymus and thymoma are reported by Gutsche et al [16].

Low Levels of Acetylcholine Receptor Delta-Subunit Message and Protein in Human Thymus Suggests the Occurrence of ‘Triplet Receptors’ in Thymic Myoid Cells

Myasthenia gravis (MG) is an autoimmune disease caused by autoantibodies against the acetylcholine receptor (AChR) at the neuromuscular junction [1, 2]. Mature CD4+ T-cells are involved in the production of these antibodies [3, 4]. The destruction at the neuromuscular endplates leads to the clinical symptom of muscle weakness.

Abnormal Thymocyte Development and Neurofilament-Reactive Thymocytes in Thymoma

Myasthenia gravis (MG) is an autoimmune disease caused by autoantibodies against the acetylcholine receptor (AChR) at the neuromuscular junction [1]. The muscular AChR has been extensively characterized [2], but the etiology of MG is still obscure. Whether the muscular AChR or another (auto)antigen plays a role during the initiation of MG is unknown [3]. The muscular AChR is a pentameric ion channel composed of four different subunits. The α-subunit contains the acetylcholine binding site and the main epitopes recognized by MG autoantibodies [2]. The human muscle AChR α-subunit exists as two isoforms, P3A- and P3A+ [4]. This is a result of alternative splicing of the P3A exon located between exons three and four. The P3A+ isoform does not bind α-bungarotoxin or monoclonal antibodies against the AChR main immunogenic region and is not integrated into functional AChR [5]. The muscular AChR belongs to the family of nicotinic AChRs as do neuronal AChRs. Since muscular and neuronal AChRs share significant molecular homology [6], neuronal AChRs have been considered as candidate autoantigens able to elicit autoimmunity against the muscular AChR by molecular mimicry [7].

Expression of the Acetylcholine Receptor α-Subunit Gene is Associated with Paraneoplastic Myasthenia Gravis in Mixed Thymoma

http://link.springer.com/content/pdf/10.1007/978-94-011-4060-7_6.pdf

6. Abnormol Thymocyte Dcoclopmcnt and Neurofilament-Reactive Thbmocytcs in TbbIDomo

Paraneoplastic myasthenia gravis correlates with generation of mature naive CD4+ T cells in thymomas

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