A case of vitiligo after COVID-19 vaccination: a possible role of thymic dysfunction. / 一例由2019å† ç— æ¯’ç— (COVID-19)ç–«è‹—æŽ¥ç§å¼•å‘çš„ç™½ç™œé£Žç— ä¾‹åŠå ¶èƒ¸è ºåŠŸèƒ½éšœç¢çš„ä½œç”¨æœºåˆ¶åˆ†æž.

During the coronavirus disease 2019 (COVID-19) pandemic, vaccines help control the spread of infection. To date, 47 vaccines have been approved, with another 227 candidates in various stages of development. In the short period of time since the beginning of their use, evidence has begun to emerge of complications following vaccination in the form of the development or exacerbation of a number of pathological conditions (Block et al., 2022; Haseeb et al., 2022). For example, a population-based study in France identified 1612 cases of myocarditis and 1613 cases of pericarditis requiring hospital treatment within five months of vaccination (le Vu et al., 2022).

Lead induced thymic immunosuppression in Japanese quail (Coturnix japonica) via oxidative stress-based T cell receptor pathway signaling inhibition.

The human-induced lead (Pb) contamination brings about serious environmental issues around the world and it also poses severe risks to wildlife including birds. Avian thymus is one of primary lymphoid organs and it plays an important role in regulating T cell-based cellular immunity. Therefore, in this study, we tried to examine toxic effects and potential molecular mechanism of Pb on avian thymus using a biological model species-Japanese quail (Coturnix japonica). One-week-old Japanese quails were exposed to 0, 50, 500 and 1000 ppm Pb concentrations in drinking water for three weeks when thymus reached developmental climax. The results showed body weight, thymus weight and thymic size were reduced significantly by Pb exposure. Meanwhile, histopathological changes including vacuolation, cortex atrophy and nuclear debris were detected in thymic cells of Pb exposure. In addition, ultrastructural alterations such as mitochondrial damage, chromatin condensation, and nuclear destruction were found in the thymus of Pb treatments. The increase of reactive oxygen species (ROS) and Malondialdehyde (MDA) as well as the inhibition of antioxidant system indicated that Pb exposure caused oxidative damages in the thymus. Pb exposure also increased thymic cell apoptosis. Moreover, RNA-Seq analysis revealed that thymic functional pathways were disrupted by Pb exposure. Especially, Pb exposure disturbed T cell differentiation and led to T helper type 1 (Th1) /T helper type 2 (Th2) imbalance by interfering with T cell receptor signaling and cytokine signaling. This study implied that Pb caused thymic immunosuppression through causing morphological deformation, structural destruction, oxidation and molecular signaling disruption.

Hallmarks of T cell aging.

The aged adaptive immune system is characterized by progressive dysfunction as well as increased autoimmunity. This decline is responsible for elevated susceptibility to infection and cancer, as well as decreased vaccination efficacy. Recent evidence indicates that CD4+ T cell-intrinsic alteratins contribute to chronic inflammation and are sufficient to accelerate an organism-wide aging phenotype, supporting the idea that T cell aging plays a major role in body-wide deterioration. In this Review, we propose ten molecular hallmarks to represent common denominators of T cell aging. These hallmarks are grouped into four primary hallmarks (thymic involution, mitochondrial dysfunction, genetic and epigenetic alterations, and loss of proteostasis) and four secondary hallmarks (reduction of the TCR repertoire, naive-memory imbalance, T cell senescence, and lack of effector plasticity), and together they explain the manifestation of the two integrative hallmarks (immunodeficiency and inflammaging). A major challenge now is weighing the relative impact of these hallmarks on T cell aging and understanding their interconnections, with the final goal of defining molecular targets for interventions in the aging process.

Thymic Aging May Be Associated with COVID-19 Pathophysiology in the Elderly.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the global pandemic of coronavirus disease 2019 (COVID-19) and particularly exhibits severe symptoms and mortality in elderly individuals. Mounting evidence shows that the characteristics of the age-related clinical severity of COVID-19 are attributed to insufficient antiviral immune function and excessive self-damaging immune reaction, involving T cell immunity and associated with pre-existing basal inflammation in the elderly. Age-related changes to T cell immunosenescence is characterized by not only restricted T cell receptor (TCR) repertoire diversity, accumulation of exhausted and/or senescent memory T cells, but also by increased self-reactive T cell- and innate immune cell-induced chronic inflammation, and accumulated and functionally enhanced polyclonal regulatory T (Treg) cells. Many of these changes can be traced back to age-related thymic involution/degeneration. How these changes contribute to differences in COVID-19 disease severity between young and aged patients is an urgent area of investigation. Therefore, we attempt to connect various clues in this field by reviewing and discussing recent research on the role of the thymus and T cells in COVID-19 immunity during aging (a synergistic effect of diminished responses to pathogens and enhanced responses to self) impacting age-related clinical severity of COVID-19. We also address potential combinational strategies to rejuvenate multiple aging-impacted immune system checkpoints by revival of aged thymic function, boosting peripheral T cell responses, and alleviating chronic, basal inflammation to improve the efficiency of anti-SARS-CoV-2 immunity and vaccination in the elderly.

When the Damage Is Done: Injury and Repair in Thymus Function.

Even though the thymus is exquisitely sensitive to acute insults like infection, shock, or common cancer therapies such as cytoreductive chemo- or radiation-therapy, it also has a remarkable capacity for repair. This phenomenon of endogenous thymic regeneration has been known for longer even than its primary function to generate T cells, however, the underlying mechanisms controlling the process have been largely unstudied. Although there is likely continual thymic involution and regeneration in response to stress and infection in otherwise healthy people, acute and profound thymic damage such as that caused by common cancer cytoreductive therapies or the conditioning regimes as part of hematopoietic cell transplantation (HCT), leads to prolonged T cell deficiency; precipitating high morbidity and mortality from opportunistic infections and may even facilitate cancer relapse. Furthermore, this capacity for regeneration declines with age as a function of thymic involution; which even at steady state leads to reduced capacity to respond to new pathogens, vaccines, and immunotherapy. Consequently, there is a real clinical need for strategies that can boost thymic function and enhance T cell immunity. One approach to the development of such therapies is to exploit the processes of endogenous thymic regeneration into novel pharmacologic strategies to boost T cell reconstitution in clinical settings of immune depletion such as HCT. In this review, we will highlight recent work that has revealed the mechanisms by which the thymus is capable of repairing itself and how this knowledge is being used to develop novel therapies to boost immune function.

Ageing compromises mouse thymus function and remodels epithelial cell differentiation.

Ageing is characterised by cellular senescence, leading to imbalanced tissue maintenance, cell death and compromised organ function. This is first observed in the thymus, the primary lymphoid organ that generates and selects T cells. However, the molecular and cellular mechanisms underpinning these ageing processes remain unclear. Here, we show that mouse ageing leads to less efficient T cell selection, decreased self-antigen representation and increased T cell receptor repertoire diversity. Using a combination of single-cell RNA-seq and lineage-tracing, we find that progenitor cells are the principal targets of ageing, whereas the function of individual mature thymic epithelial cells is compromised only modestly. Specifically, an early-life precursor cell population, retained in the mouse cortex postnatally, is virtually extinguished at puberty. Concomitantly, a medullary precursor cell quiesces, thereby impairing maintenance of the medullary epithelium. Thus, ageing disrupts thymic progenitor differentiation and impairs the core immunological functions of the thymus.

Uremia-Associated Ageing of the Thymus and Adaptive Immune Responses.

Progressive loss of renal function is associated with a series of changes of the adaptive immune system which collectively constitute premature immunological ageing. This phenomenon contributes significantly to the mortality and morbidity of end-stage renal disease (ESRD) patients. In this review, the effect of ESRD on the T cell part of the adaptive immune system is highlighted. Naïve T cell lymphopenia, in combination with the expansion of highly differentiated memory T cells, are the hallmarks of immunological ageing. The decreased production of newly formed T cells by the thymus is critically involved. This affects both the CD4 and CD8 T cell compartment and may contribute to the expansion of memory T cells. The expanding populations of memory T cells have a pro-inflammatory phenotype, add to low-grade inflammation already present in ESRD patients and destabilize atherosclerotic plaques. The effect of loss of renal function on the thymus is not reversed after restoring renal function by kidney transplantation and constitutes a long-term mortality risk factor. Promising results from animal experiments have shown that rejuvenation of the thymus is a possibility, although not yet applicable in humans.

Implications of Oxidative Stress and Cellular Senescence in Age-Related Thymus Involution.

The human thymus is a primary lymphoepithelial organ which supports the production of self-tolerant T cells with competent and regulatory functions. Paradoxically, despite the crucial role that it exerts in T cell-mediated immunity and prevention of systemic autoimmunity, the thymus is the first organ of the body that exhibits age-associated degeneration/regression, termed "thymic involution." A hallmark of this early phenomenon is a progressive decline of thymic mass as well as a decreased output of naïve T cells, thus resulting in impaired immune response. Importantly, thymic involution has been recently linked with cellular senescence which is a stress response induced by various stimuli. Accumulation of senescent cells in tissues has been implicated in aging and a plethora of age-related diseases. In addition, several lines of evidence indicate that oxidative stress, a well-established trigger of senescence, is also involved in thymic involution, thus highlighting a possible interplay between oxidative stress, senescence, and thymic involution.

Interim thymus and activation regulated chemokine versus interim 18 F-fluorodeoxyglucose positron-emission tomography in classical Hodgkin lymphoma response evaluation.

Serum thymus and activation regulated chemokine (TARC) levels reflect classical Hodgkin lymphoma (cHL) disease activity and correspond with treatment response. We compared mid-treatment interim TARC (iTARC) with interim 18 F-fluorodeoxyglucose positron-emission tomography (iPET) imaging to predict modified progression-free survival (mPFS) in a group of 95 patients with cHL. High iTARC levels were found in nine and positive iPET in 17 patients. The positive predictive value (PPV) of iTARC for a 5-year mPFS event was 88% compared to 47% for iPET. The negative predictive value was comparable at 86% for iTARC and 85% for iPET. Serum iTARC levels more accurately reflect treatment response with a higher PPV compared to iPET.

Janus kinase inhibitor ruxolitinib blocks thymic regeneration after acute thymus injury.

Thymic epithelial cells (TECs) are crucial for the production of T-cells. Cancer therapies including cytotoxic drugs and ionizing radiations damage TECs resulting in abnormal T-cell production and function. Fortunately, TECs can regenerate after injury. The Janus kinase (Jak) pathway is important in supporting survival of TECs. Jak inhibitors are used to treat cancer and immune disorders. The impact of Jak inhibitors on recovery of TECs is unknown. We induced acute thymus injury in mice by using ionizing radiation and evaluated the impact of ruxolitinib on thymus regeneration. We also tested if ruxolitinib affected proliferation of TECs in vitro. An increase was observed in the recovery of thymus cells after acute injury in association with up-regulation of TEC-related growth factors including keratinocyte growth factor (Kgf), epidermal growth factor (Egf), insulin-like growth factor 1 (Igf1) and receptor activator of NF-κB ligand (Rankl). Giving ruxolitinib decreased levels of receptors of these growth factors on TECs and blocked growth factor-induced recovery of thymus cells in damaged thymii. Ruxolitinib also blocked growth factors-induced proliferation of TECs in vitro. Thymus regeneration was inhibited when ruxolitinib was given immediately after thymus injury but not when it was given 1 week later. These data may have implications for how ruxolitinib is used in clinical practices.

Prenatal and childhood exposures are associated with thymulin concentrations in young adolescent children in rural Nepal.

The thymus undergoes a critical period of growth and development early in gestation and, by mid-gestation, immature thymocytes are subject to positive and negative selection. Exposure to undernutrition during these periods may permanently affect phenotype. We measured thymulin concentrations, as a proxy for thymic size and function, in children (n = 290; aged 9-13 years) born to participants in a cluster-randomized trial of maternal vitamin A or ß-carotene supplementation in rural Nepal (1994-1997). The geometric mean (95% confidence interval) thymulin concentration was 1.37 ng/ml (1.27, 1.47). A multivariate model of early-life exposures revealed a positive association with gestational age at delivery (ß = 0.02; P = 0.05) and higher concentrations among children born to ß-carotene-supplemented mothers (ß = 0.19; P < 0.05). At ∼9-12 years of age, thymulin was positively associated with all anthropometric measures, with height retained in our multivariate model (ß = 0.02; P < 0.001). There was significant seasonal variation: concentrations tended to be lower pre-monsoon (ß = -0.13; P = 0.15), during the monsoon (ß = -0.22; P = 0.04), and pre-harvest (ß = -0.34; P = 0.01), relative to the post-harvest season. All early-life associations, except supplementation, were mediated in part by nutritional status at follow-up. Our findings underscore the known sensitivity of the thymus to nutrition, including potentially lasting effects of early nutritional exposures. The relevance of these findings to later disease risk remains to be explored, particularly given the role of thymulin in the neuroendocrine regulation of inflammation.

Trans-omics Impact of Thymoproteasome in Cortical Thymic Epithelial Cells.

The thymic function to produce self-protective and self-tolerant T cells is chiefly mediated by cortical thymic epithelial cells (cTECs) and medullary TECs (mTECs). Recent studies including single-cell transcriptomic analyses have highlighted a rich diversity in functional mTEC subpopulations. Because of their limited cellularity, however, the biochemical characterization of TECs, including the proteomic profiling of cTECs and mTECs, has remained unestablished. Utilizing genetically modified mice that carry enlarged but functional thymuses, here we show a combination of proteomic and transcriptomic profiles for cTECs and mTECs, which identified signature molecules that characterize a developmental and functional contrast between cTECs and mTECs. Our results reveal a highly specific impact of the thymoproteasome on proteasome subunit composition in cTECs and provide an integrated trans-omics platform for further exploration of thymus biology.

Dynamics of T cell receptor distributions following acute thymic atrophy and resumption.

Naive human T cells are produced and developed in the thymus, which atrophies abruptly and severely in response to physical or psychological stress. To understand how an instance of stress affects the size and "diversity" of the peripheral naive T cell pool, we derive a mean-field autonomous ODE model of T cell replenishment that allows us to track the clone abundance distribution (the mean number of different TCRs each represented by a specific number of cells). We identify equilibrium solutions that arise at different rates of T cell production, and derive analytic approximations to the dominant eigenvalues and eigenvectors of the mathematical model linearized about these equilibria. From the forms of the eigenvalues and eigenvectors, we estimate rates at which counts of clones of different sizes converge to and depart from equilibrium values-that is, how the number of clones of different sizes "adjusts" to the changing rate of T cell production. Under most physiological realizations of our model, the dominant eigenvalue (representing the slowest dynamics of the clone abundance distribution) scales as a power law in the thymic output for low output levels, but saturates at higher T cell production rates. Our analysis provides a framework for quantitatively understanding how the clone abundance distribution evolves under small changes in the overall T cell production rate.

Epigenetic Age Reversal by Cell-Extrinsic and Cell-Intrinsic Means.

Reversal of aging by factors or drugs that reprogram adult cells to induced pluripotent stem cells suggests that at least at the cellular level aging may be reversible by resetting somatic cell state to a "ground state." An open question has been whether such rejuvenation is possible in whole organisms, especially in mammals. A related key question is whether rejuvenation can be dissociated from dedifferentiation. Several recent reports suggest that one prominent biomarker of mammalian aging, age-associated DNA methylation (DNAm) state that has been used to create DNAm age (DNAma) clocks, can be partially reversed by intrinsic treatment of cells with sets of reprogramming factors without affecting cell fate. Partial reprogramming using a superset of reprogramming factors applied transiently or subset of Yamanaka factors applied continually can increase regenerative potential, and reverse DNAma, while maintaining cell identity. Alternatively, a cell-extrinsic manipulation can accomplish something similar. A small preliminary clinical trial in humans suggests that systemic treatment with a cocktail of growth hormone, dehydroepiandrosterone, and metformin could also partially reverse DNAma and at the same time regenerate the thymus, which shrinks with age. Important questions are raised: How completely does reversing DNAma clocks embody a reversal of other age-related phenotypes, such as functional decline in strength, cognition, or immunity? How universal are these epigenetic changes at the tissue and cell levels? For example, do populations of younger stem cells exist that respond to these manipulations and then only confer the appearance of decreasing DNAma as they proliferate and differentiate? Together, these studies have profound implications for the development of antiaging and healthspan-enhancing therapies. A combination of both intrinsic and extrinsic modalities will most likely provide an optimal benefit.

State of Stress-Marker Organs in Rats after a Single Exposure to Long-Term Stress and Treatment with Lipopolysaccharide.

We studied the effect of LPS on the state of stress-marker organs in rats at various periods after a single exposure to long-term stress on the model of 24-h immobilization. The animals were intraperitoneally injected with LPS in a dose of 100 µg/kg immediately after the negative emotiogenic exposure. Changes in physiological parameters were evaluated 3 h, 1 day, and 8 days after immune stimulation. Acute stress was accompanied by a decrease in the weight of the thymus during all stages of the post-stress period. An increase in the relative weight of theadrenal glands in animals under these conditions was observed only on day 8 after restraint stress. The induction of immune reactions due to systemic treatment with LPS was shown to prevent involution of the spleen in the late stage after a single exposure to long-term stress (day 8). Hypertrophy of the adrenal glands, which serves as one of the typical reactions of mammals to negative emotiogenic factors, was not revealed during the post-stress period after antigenic stimulation. These data hold much promise for the development of new approaches to the use of immunoactive substances to prevent or reduce the severity of physiological changes after emotiogenic loads.

Dynamic changes in epithelial cell morphology control thymic organ size during atrophy and regeneration.

T lymphocytes must be produced throughout life, yet the thymus, where T lymphocytes are made, exhibits accelerated atrophy with age. Even in advanced atrophy, however, the thymus remains plastic, and can be regenerated by appropriate stimuli. Logically, thymic atrophy is thought to reflect senescent cell death, while regeneration requires proliferation of stem or progenitor cells, although evidence is scarce. Here we use conditional reporters to show that accelerated thymic atrophy reflects contraction of complex cell projections unique to cortical epithelial cells, while regeneration requires their regrowth. Both atrophy and regeneration are independent of changes in epithelial cell number, suggesting that the size of the thymus is regulated primarily by rate-limiting morphological changes in cortical stroma, rather than by their cell death or proliferation. Our data also suggest that cortical epithelial morphology is under the control of medullary stromal signals, revealing a previously unrecognized endocrine-paracrine signaling axis in the thymus.

Enfermedades del timo por exceso y por defecto / Thymus diseases by excess and default

El timo es un órgano cervicotorácico, impar y mediano, situado en la base del cuello y parte superior del mediastino. Junto a la médula ósea es uno de los dos órganos primarios del sistema inmune y ejerce su función en los neonatos y en los niños, fundamentalmente. Entra en regresión a partir de la pubertad, aunque algunos autores plantean que la involución puede comenzar un poco antes, cuando los principales tejidos linfoides están plenamente desarrollados. Interviene sinérgicamente con otras glándulas de secreción interna: tiroides, suprarrenal, hipófisis, para elaborar substancias necesarias para el desarrollo general del organismo. Es un órgano muy sensible a todo influjo. Como todos los órganos de la economía el timo presenta enfermedades producidas tanto por crecimiento exagerado, como por hipoplasias o atrofias. Dentro de las primeras las más comunes son la hiperplasia tímica y el timoma y, entre las últimas el síndrome de DiGeorge ha sido bien caracterizado en la literatura internacional desde la segunda mitad del siglo pasado. Sin embrago, en los últimos tiempos los inmunólogos hablan de la hipoplasia tímica como entidad que puede asociarse o no a estados de inmunodeficiencia. Se describen brevemente estas afecciones(AU)

The thymus is a cervicothoracic organ, odd and medium, located at the base of the neck and upper part of the mediastinum. Next to the bone marrow is one of the two primary organs of the immune system and exerts its function in neonates and children, fundamentally. It regresses after puberty, although some authors suggest that the involution can begin a little earlier, when the main lymphoid tissues are fully developed. It intervenes synergistically with other glands of internal secretion: thyroid, adrenal, pituitary gland, to develop substances necessary for the general development of the organism. It is a very sensitive organ to all influence. Like all the organs of the economy, the thymus presents diseases caused both by exaggerated growth, as by hypoplasias or atrophies. Among the former, the most common are thymic hyperplasia and thymoma and, among the latter, DiGeorge syndrome has been well characterized in international literature since the second half of the last century. However, in recent times immunologists speak of thymic hypoplasia as an entity that may or may not be associated with immunodeficiency states. These conditions are briefly described(AU)

El timoma, ¿es una enfermedad sistémica? / Thymoma. A Systemic Disease?

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The role of thymus preservation in parathyroid gland function and surgical completeness after bilateral central lymph node dissection for papillary thyroid cancer: A randomized controlled study.

BACKGROUND: The clinical value of thymus preservation during thyroid carcinoma surgery remains unclear. The aim of this study is to explore the role of bilateral thymus preservation in parathyroid glands (PGs) function and surgical completeness in total thyroidectomy (TT) with bilateral central lymph node dissection (CLND). MATERIALS AND METHODS: Fifty-four consecutive patients who underwent TT and bilateral CLND were assigned to the thymus preservation (TP) group (n = 27) and the bilateral thymectomy (BT) group (n = 27). Surgical completeness was evaluated by the number of lymph nodes dissected, serum Tg level and ultrasound findings postoperatively. RESULTS: Incidental parathyroidectomy was more common in the BT group (29.6% vs 7.4%, p = 0.038). Patients in the BT group had higher risks of neuromuscular symptoms (63.0% vs 29.6%, P = 0.014) and transient hypoparathyroidism (70.4% vs 25.9%, P = 0.001). The incidence of persistent hypoparathyroidism failed to show a significant difference between the TP and BT groups (0 vs 14.8%, P = 0.111). However, those with transient hypoparathyroidism in the BT group had a lower level of serum PTH at 3 weeks postoperatively (p = 0.001). There was no significant difference in the number of lymph nodes dissected (5.89 ±â€¯3.12 vs 8.56 ±â€¯6.93, P = 0.077) and preablation sTg level (1.82 ±â€¯2.18 vs 1.42 ±â€¯1.56 ng/ml, P = 0.775) between the TP and BT groups. No metastatic lymph nodes were found on sonography at 3 months postoperatively in both groups. CONCLUSION: Thymus preservation had benefits on protecting PGs and promoting rapid clinical resolution of hypoparathyroidism. It had no effects on oncologic completeness of TT with bilateral CLND.

Genetic characterization of thymoma.

Thymoma represents the most common anterior mediastinal compartment neoplasm, originating from the epithelial cell population in the thymus. Various histological types of thymoma feature different clinical characteristics. Furthermore, thymoma is frequently associated with autoimmune disorders, esp. myasthenia gravis (MG). However, the underlying molecular tumourigenesis of thymoma remains largely unknown. The goal of our current study is to demonstrate the underlying genetic abberations in thymoma, so as to understand the possible cause of MG in thymoma patients. By using CapitalBio mRNA microarray analysis, we analyzed 31 cases of thymoma including 5 cases of type AB thymoma, 6 B1-type cases, 12 B2-type cases, 5 B2B3-type cases and 3 type-B3 cases. 6 cases of thymoma were not associated with myasthenia gravis, while 25 cases were with myasthenia gravis. By comparisons between thymoma and the paratumoral tissues, differentially expressed genes were identified preliminarily. Among them, 292 genes increased more than 2-fold, 2 genes more than 5-fold. On the other hand, 596 genes were decreased more than 2-fold, 6 genes more than 20-fold. Interestingly, among these genes upregulated more than 2-fold, 6 driver genes (FANCI, NCAPD3, NCAPG, OXCT1, EPHA1 and MCM2) were formerly reported as driver oncogenes. This microarray results were further confirmed through real-time PCR. 8 most dysregulated genes were verified: E2F2, EPHA1, CCL25 and MCM2 were upregulated; and IL6, FABP4, CD36 and MYOC were downregulated. Supervised clustering heat map analysis of 2-fold upregulated and 2-fold downregulated genes revealed 6 distinct clusters. Strikingly, we found that cluster 1 was composed of two type-B2 thymoma; and cluster 6 was three type-B2/B3 thymoma. KEGG database analysis revealed possible genetic mechanisms of thymoma and functional process. We further compared gene expression pattern between thymoma with and without MG, and found 5 genes were upregulated more than 2-fold, more than 30 genes were downregulated more than 2-fold. KEGG analysis revealed 2 important signaling pathways with more than 2-fold upregulated genes (TGF- beta signaling pathway and HTLV-I signaling pathway) as differially functioning between MG positive and negative thymomas. Real-time PCR analysis confirmed that CCL25 was upregulated; and MYC, GADD45B, TNFRSF12 downregulated in thymoma with MG. Our study thus provided important genetic information on thymoma. It shed light on the molecular bases for analyzing the functional process of thymoma and finding potential biomarkers for pathological categorizing and treatment. Our work may provide important clues in understanding possible causes of MG in thymoma patients.