Accelerated thymic atrophy as a result of elevated homeostatic expression of the genes encoded by the TNF/lymphotoxin cytokine locus

2009 ◽  
Vol 39 (10) ◽  
pp. 2906-2915 ◽  
Author(s):  
Dmitry J. Liepinsh ◽  
Andrei A. Kruglov ◽  
Arthur R. Galimov ◽  
Alexander N. Shakhov ◽  
Yuriy V. Shebzukhov ◽  
...  
Keyword(s):  
Thymic Atrophy

Thymic atrophy creates holes in Treg‐mediated immuno‐regulation via impairment of an antigen‐specific clone

Immunology ◽  
2021 ◽  
Author(s):  
Rachel Thomas ◽  
Jiyoung Oh ◽  
Weikan Wang ◽  
Dong‐Ming Su
Keyword(s):  
Thymic Atrophy

VEGF inhibits T-cell development and may contribute to tumor-induced immune suppression

Blood ◽  
2003 ◽  
Vol 101 (12) ◽  
pp. 4878-4886 ◽  
Author(s):  
Joyce E. Ohm ◽  
Dmitry I. Gabrilovich ◽  
Gregory D. Sempowski ◽  
Ekaterina Kisseleva ◽  
Kelly S. Parman ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Cancer Patients ◽  
Thymocyte Development ◽  
Thymic Atrophy ◽  
Fetal Thymic Organ Culture ◽  
Immune Deficiencies ◽  
Thymocyte Apoptosis ◽  
Advanced Stage Cancer ◽  
Endothelial Growth Factor

AbstractT-cell defects and premature thymic atrophy occur in cancer patients and tumor-bearing animals. We demonstrate that exposure of mice to recombinant vascular endothelial growth factor (VEGF) at concentrations similar to those observed in advanced stage cancer patients reproduces this profound thymic atrophy and is highlighted by a dramatic reduction in CD4+/CD8+ thymocytes. We find that VEGF does not induce thymocyte apoptosis, but instead rapidly decreases the number of the earliest observable progenitors in the thymus. VEGF does not inhibit thymocyte development in fetal thymic organ culture, further suggesting a prethymic effect. We also demonstrate that bone marrow progenitors from animals infused with recombinant VEGF and transferred to irradiated untreated animals recolonize the thymus more efficiently than progenitors from control animals. This suggests that VEGF exposure is associated with an increased population of thymus-committed progenitors in the bone marrow. We hypothesize that pathophysiologically relevant concentrations of VEGF may block the differentiation and/or emigration of these progenitors resulting in the observed thymic atrophy. Removal of VEGF via cessation of infusion or adoptive transfer of progenitors to a congenic host induces a preferential commitment of lymphoid progenitors to the T lineage and results in a restoration of the normal composition and cellularity of the thymus. These data demonstrate that at pathophysiologic concentrations, VEGF interferes with the development of T cells from early hematopoetic progenitor cells and this may contribute to tumor-associated immune deficiencies.

Thymic atrophy induced by acute exposure of 3,3′,4,4′-tetrachloroazobenzene and 3,3′4,4′-tetrachloroazoxy-benzene in rats

Toxicology ◽  
1982 ◽  
Vol 24 (3-4) ◽  
pp. 231-244 ◽  
Author(s):  
M.T. Stephen Hsia ◽  
Charles F. Burant ◽  
Bill L. Kreamer ◽  
Kenneth R. Schrankel
Keyword(s):  
Acute Exposure ◽  
Thymic Atrophy

Effects of Subchronic Exposure of Rats to 2-Methoxyethanol or 2-Butoxyethanol: Thymic Atrophy and Immunotoxicity

1991 ◽  
Vol 16 (4) ◽  
pp. 830-840 ◽  
Author(s):  
JERRY H. EXON ◽  
GARY G. MATHER ◽  
JEANINE L. BUSSIERE ◽  
DAVID P. OLSON ◽  
PATRICIA A. TALCOTT
Keyword(s):  
Thymic Atrophy ◽  
Subchronic Exposure

Parathyroidectomy and the induction of thymic atrophy in normal, adrenalectomized and orchidectomized rats

1970 ◽  
Vol 76 (2) ◽  
pp. 141-149 ◽  
Author(s):  
A. D. Perris ◽  
L. A. Weiss ◽  
J. F. Whitfield
Keyword(s):  
Thymic Atrophy

scholarly journals Moloney Murine Leukemia Virus-Induced Preleukemic Thymic Atrophy and Enhanced Thymocyte Apoptosis Correlate with Disease Pathogenicity

1999 ◽  
Vol 73 (3) ◽  
pp. 2434-2441 ◽  
Author(s):  
Christine Bonzon ◽  
Hung Fan
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Annexin V ◽  
Moloney Murine Leukemia Virus ◽  
Wild Type ◽  
Thymic Atrophy ◽  
Thymocyte Apoptosis ◽  
Mink Cell ◽  
Nih Swiss ◽  
Murine Leukemia

ABSTRACT Moloney murine leukemia virus (M-MuLV) is a replication-competent, simple retrovirus that induces T-cell lymphoma with a mean latency of 3 to 4 months. During the preleukemic period (4 to 10 weeks postinoculation) a marked decrease in thymic size is apparent for M-MuLV-inoculated mice in comparison to age-matched uninoculated mice. We were interested in studying whether the thymic regression was due to an increased rate of thymocyte apoptosis in the thymi of M-MuLV-inoculated mice. Neonatal NIH/Swiss mice were inoculated subcutaneously (s.c.) with wild-type M-MuLV (approximately 105 XC PFU). Mice were sacrificed at 4 to 11 weeks postinoculation. Thymic single-cell suspensions were prepared and tested for apoptosis by two-parameter flow cytometry. Indications of apoptosis included changes in cell size and staining with 7-aminoactinomycin D or annexin V. The levels of thymocyte apoptosis were significantly higher in M-MuLV-inoculated mice than in uninoculated control animals, and the levels of apoptosis were correlated with thymic atrophy. To test the relevance of enhanced thymocyte apoptosis to leukemogenesis, mice were inoculated with the Mo+PyF101 enhancer variant of M-MuLV. When inoculated intraperitoneally, a route that results in wild-type M-MuLV leukemogenesis, mice displayed levels of enhanced thymocyte apoptosis comparable to those seen with wild-type M-MuLV. However, in mice inoculated s.c., a route that results in attenuated leukemogenesis, significantly lower levels of apoptosis were observed. This supported a role for higher levels of thymocyte apoptosis in M-MuLV leukemogenesis. To examine the possible role of mink cell focus-forming (MCF) recombinant virus in raising levels of thymocyte apoptosis, MCF-specific focal immunofluorescence assays were performed on thymocytes from preleukemic mice inoculated with M-MuLV and Mo+PyF101 M-MuLV. The results indicated that infection of thymocytes by MCF virus recombinants is not required for the increased level of apoptosis and thymic atrophy.

scholarly journals Infection-Associated Thymic Atrophy

2021 ◽  
Vol 12 ◽  
Author(s):  
Mingli Luo ◽  
Lingxin Xu ◽  
Zhengyu Qian ◽  
Xi Sun
Keyword(s):  
Immune System ◽  
T Cell Receptor ◽  
Essential Role ◽  
Cell Receptor ◽  
Vital Organ ◽  
Thymocyte Development ◽  
Thymic Atrophy ◽  
Neural Modulation ◽  
Future Work ◽  
The Impact

The thymus is a vital organ of the immune system that plays an essential role in thymocyte development and maturation. Thymic atrophy occurs with age (physiological thymic atrophy) or as a result of viral, bacterial, parasitic or fungal infection (pathological thymic atrophy). Thymic atrophy directly results in loss of thymocytes and/or destruction of the thymic architecture, and indirectly leads to a decrease in naïve T cells and limited T cell receptor diversity. Thus, it is important to recognize the causes and mechanisms that induce thymic atrophy. In this review, we highlight current progress in infection-associated pathogenic thymic atrophy and discuss its possible mechanisms. In addition, we discuss whether extracellular vesicles/exosomes could be potential carriers of pathogenic substances to the thymus, and potential drugs for the treatment of thymic atrophy. Having acknowledged that most current research is limited to serological aspects, we look forward to the possibility of extending future work regarding the impact of neural modulation on thymic atrophy.

scholarly journals Strain differences in thymic atrophy in rats immunized for EAE correlate with the clinical outcome of immunization

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0201848 ◽  
Author(s):  
Mirjana Nacka-Aleksić ◽  
Marija Stojanović ◽  
Ivan Pilipović ◽  
Zorica Stojić-Vukanić ◽  
Duško Kosec ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Strain Differences ◽  
Thymic Atrophy
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