Studies on the maturation of thymus stem cells The effects of catecholamines, histamine and peptide hormones on the expression of T cell alloantigens

Singh, Upendra; Owen, J. J. T.

doi:10.1002/eji.1830060113

Cited by 89 publications

(30 citation statements)

References 11 publications

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“…Early studies in the 1970s and 1980s allude to β-AR-induced enhancement of thymocyte differentiation and suppression of thymocyte proliferation in the presence of intact NA innervation [58][59][60][61][62][63]. Isoproterenol exposure in vivo reduces thymic weight and thymocyte number in mice [64].…”

Section: Sympathetic Neurotransmission In the Thymusmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

223

185

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Optimal host defense against pathogens requires cross-talk between the nervous and immune systems. This paper reviews sympathetic-immune interaction, one major communication pathway, and its importance for health and disease. Sympathetic innervation of primary and secondary immune organs is described, as well as evidence for neurotransmission with cells of the immune system as targets. Most research thus far as focused on neural-immune modulation in secondary lymphoid organs, and have revealed complex sympathetic modulation resulting in both potentiation and inhibition of immune functions. SNS-immune interaction may enhance immune readiness during disease-or injury-induced 'fight' responses. Research also indicate that dysregulation of the SNS can significantly affect the progression of immune-mediated diseases. However, a better understanding of neural-immune interactions is needed to develop strategies for treatment of immune-mediated diseases that are designed to return homeostasis and restore normal functioning neural-immune networks.

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Section: Sympathetic Neurotransmission In the Thymusmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

223

185

View full text Add to dashboard Cite

show abstract

“…Tracing analysis indicates that thymic sympathetic outflow directly starts in neurons from the thoracic spinal cord, brainstem, caudal raphe nucleus, and hypothalamus (Trotter et al, 2007). Furthermore, the neurotransmitter norepinephrine (Singh and Owen, 1976;Felten et al, 1987;Morale et al, 1992;Tsao et al, 1996;Kurz et al, 1997;von Patay et al, 1998von Patay et al, , 1999 is found in the thymus, and thymic cells express both ␤1-and ␤2-adrenergic receptors (Morale et al, 1992;Kurz et al, 1997;von Patay et al 1999) able to modulate maturation of T precursor cells and influence the thymic microenvironment. Thus, a link between the brain and the thymus is supported at different levels.…”

Section: Autonomic Denervation Of the Gld Thymusmentioning

confidence: 99%

Autonomic Denervation of Lymphoid Organs Leads to Epigenetic Immune Atrophy in a Mouse Model of Krabbe Disease

Galbiati¹,

Basso²,

Cantuti³

et al. 2007

J. Neurosci.

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Lysosomal ␤-galactosylceramidase deficiency results in demyelination and inflammation in the nervous system causing the neurological Krabbe disease. In the Twitcher mouse model of this disease, we found that neurological symptoms parallel progressive and severe lymphopenia. Although lymphopoiesis is normal before disease onset, primary and secondary lymphoid organs progressively degenerate afterward. This occurs despite preserved erythropoiesis and leads to severe peripheral lymphopenia caused by reduced numbers of T cell precursors and mature lymphocytes. Hematopoietic cell replacement experiments support the existence of an epigenetic factor in mutant mice reconcilable with a progressive loss of autonomic axons that hampers thymic functionality. We propose that degeneration of autonomic nerves leads to the irreversible thymic atrophy and loss of immune-competence. Our study describes a new aspect of Krabbe disease, placing patients at risk of immune-related pathologies, and identifies a novel target for therapeutic interventions.

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“…These include studies in which the appearance ofThy-1 has been a major factor in concluding that differentiation to a "'prothymocyte" or T cell has been induced in vitro (e.g., see refs. [20][21][22]. Although in some cases additional T-cell markers (e.g., TL or Lyt) have been monitored, the possibility that these antigens too occur on activated hemopoietic progenitor cells should be formally excluded.…”

mentioning

confidence: 99%

Expression of Thy-1 antigen is not limited to T cells in cultures of mouse hemopoietic cells.

Schrader¹,

Battye²,

Scollay³

1982

Proc. Natl. Acad. Sci. U.S.A.

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Large numbers of Thy-I-positive cells were observed in cultures of bone marrow cells that had been depleted of T cells and grown for 3 to 4 days in the presence of medium conditioned by concanavalin A-activated spleen cells. Cells bearing levels of Thy-i comparable with those on the bulk of thymocytes were isolated by using the fluorescence-activated cell sorter. Although many were large blasts, the Thy-i-positive cells failed to grow in response to T-cell growth factor and concanavalin A; about one-third, however, proliferated in the presence of factors stimulating hemopoietic progenitor cells. Furthermore, the Thy-I-positive population included cells capable of forming large colonies of macrophages and granulocytes in agar and cells forming splenic colonies in lethally irradiated mice. The appearance of the Thy-i-positive cells did not correlate with the presence of either T-cell growth factor or T-cell-derived granulocyte/macrophage colony-stimulating factor. These findings indicate that Thy-i can occur on various murine hemopoietic stem and progenitor cells and myeloid cells; Thy-i can no longer be regarded as an unambiguous marker of commitment to the T-cell lineage.The Thy-i antigen was first described in the mouse, where it was shown to exist in two allelic forms, Thy-i. 1 and Thy-1.2, and to be present on neural and lymphoid tissues (1). Further studies showed that, in mice, Thy-i served as a marker for T lymphocytes (2). In the past decade, immunologists studying the mouse have regarded the presence of the Thy-i antigen as an unambiguous marker for distinguishing lymphoid cells ofthe T-cell lineage from B lymphocytes and other cells of the hemopoietic system.Here, however, we show that Thy-I antigen can be detected on a relatively large proportion ofmouse bone marrow cells after a short period of tissue culture in the presence of medium conditioned by activated T cells or a myelomonocytic line, WEHI-3B. The Thy-l-positive cells included obvious myeloid cells together with hemopoietic stem and progenitor cells; these observations place important qualifications on the validity of Thy-1 as a marker for T cells in the mouse. MATERIALS AND METHODSMice. CBA/H Wehi and AKR mice were bred under specific pathogen-free conditions at the Hall Institute.Antibodies. Monoclonal anti-Thy 1.2, 30-H12, a rat antibody (3), and monoclonal anti-Thy 1.1, HO-22-1, a mouse antibody (4), were prepared from culture supernatants. The antibodies were directly conjugated with fluorescein isothiocyanate or were used in conjunction with fluorescein-conjugated rabbit anti-mouse immunoglobulin (Fl-anti-Ig).Staining of Cells. Antibodies were centrifuged in a Beckman Airfuge prior to use to remove aggregates. Fresh thymocytes were stained in parallel as standards. Staining was carried out at 40C, and cells were washed through an underlayer of fetal calf serum.Tissue Culture-Generation of Thy-i Positive Cells. One million viable nucleated bone marrow cells were cultured in 12-well Linbro plates in 1 ml of Dulbecco's modified Eag...

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Studies on the maturation of thymus stem cells The effects of catecholamines, histamine and peptide hormones on the expression of T cell alloantigens

Cited by 89 publications

References 11 publications

Sympathetic modulation of immunity: Relevance to disease

Sympathetic modulation of immunity: Relevance to disease

Autonomic Denervation of Lymphoid Organs Leads to Epigenetic Immune Atrophy in a Mouse Model of Krabbe Disease

Expression of Thy-1 antigen is not limited to T cells in cultures of mouse hemopoietic cells.

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