Lymphotoxin gene expression by melanocytes and melanoma cell lines and persistence of unspliced mRNA

Melani, Cecilia; Silvani, Anna; Parmiani, Giorgio; Colombo, Mario P.

doi:10.1016/0014-5793(93)80451-y

Cited by 8 publications

(4 citation statements)

References 32 publications

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“…22,54 Consistent with the expression of LTb mRNA and protein in intrinsic renal cells, expression has been described by other non-hematopoietic cells, e.g., human hepatocytes, pancreatic acinar cells, melanocytes, lung epithelial cells, osteoarthritic chondrocytes, and in hepatic oval cells. 33,34,55 Localization of LTbR by immunohistochemistry and in situ hybridization showed three potential targets, i.e., parietal epithelial, tubular epithelial, and mesangial cells. The expression of LTb might contribute to a pro-inflammatory milieu via chemokine release and inflammatory cell recruitment mediated by these cells.…”

Section: Discussionmentioning

confidence: 99%

The lymphotoxin β receptor is a potential therapeutic target in renal inflammation

Seleznik

Seeger

Bauer

et al. 2016

Kidney International

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Accumulation of inflammatory cells in different renal compartments is a hallmark of progressive kidney diseases including glomerulonephritis (GN). Lymphotoxin β receptor (LTβR) signaling is crucial for the formation of lymphoid tissue, and inhibition of LTβR signaling has ameliorated several non-renal inflammatory models. Therefore, we tested whether LTβR signaling could also have a role in renal injury. Renal biopsies from patients with GN were found to express both LTα and LTβ ligands, as well as LTβR. The LTβR protein and mRNA were localized to tubular epithelial cells, parietal epithelial cells, crescents, and cells of the glomerular tuft, whereas LTβ was found on lymphocytes and tubular epithelial cells. Human tubular epithelial cells, mesangial cells, and mouse parietal epithelial cells expressed both LTα and LTβ mRNA upon stimulation with TNF in vitro. Several chemokine mRNAs and proteins were expressed in response to LTβR signaling. Importantly, in a murine lupus model, LTβR blockade improved renal function without the reduction of serum autoantibody titers or glomerular immune complex deposition. Thus, a preclinical mouse model and human studies strongly suggest that LTβR signaling is involved in renal injury and may be a suitable therapeutic target in renal diseases.

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Section: Discussionmentioning

confidence: 99%

The lymphotoxin β receptor is a potential therapeutic target in renal inflammation

Seleznik

Seeger

Bauer

et al. 2016

Kidney International

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“…LT␤R is also expressed in the thymus at this time even though a role for the LT system in thymic development or function has not been revealed in genetically deleted mice (34). The embryonic expression of LT␤ in the skin is intriguing given reports of nonlymphoid expression of LT␣ RNA or protein in inflamed epithelial layers such as in lichenoid skin, in keratinocytes from the middle ear with the hyperproliferating disease cholesteatoma, in skin following hair regression, and in melanocytes (35)(36)(37)(38). The expression of LT␣ or LT␤ in nonlymphoid/myeloid cells at sites of inflammation has not been extensively studied.…”

Section: Discussionmentioning

confidence: 99%

Visualization of Lymphotoxin-β and Lymphotoxin-β Receptor Expression in Mouse Embryos

Browning

French

2002

The Journal of Immunology

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The heteromeric lymphotoxin αβ ligand (LT) binds to the LTβ receptor (LTβR) and provides an essential trigger for lymph node (LN) development. LTβR signaling is also critical for the emergence of pathological ectopic lymph node-like structures and the maintenance of an organized splenic white pulp. To better understand the role of LT in development, the expression patterns of LTβ and LTβR mRNA were examined by in situ hybridization in the developing mouse embryo. Images of LTβ ligand expression in developing peripheral LN in the E18.5 embryo revealed a relatively early phase structure and allowed for comparative staging with LN development in rat and humans. The LTβR is expressed from E16.5 onward in respiratory, salivary, bronchial, and gastric epithelium, which may be consistent with early communication events between lymphoid elements and epithelial specialization over emerging mucosal LN. Direct comparison of mouse fetal and adult tissues by FACS analysis confirmed the elevated expression of LTBR in some embryonic epithelial layers. Therefore, surface LTBR expression may be elevated during fetal development in some epithelial layers.

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“…However, experiments aimed to exclude this possibility are underway by testing the ability of the anti–MAdCAM-1 Ab to interfere with short-term segregation of B cells in SCID mice. Because of the lack of lymphocytes in the SCID spleen, LT-α expression in nonlymphoid cells ( 32 ) or NK cells ( 32 ) must be responsible for maintaining MAdCAM-1 expression. That is surprising since expression of LT-α/β and LT-α3 is described as restricted to activated lymphocytes ( 33 – 35 ).…”

Section: Discussionmentioning

confidence: 99%

The Sequential Role of Lymphotoxin and B Cells in the Development of Splenic Follicles

González

Mackay

Browning

et al. 1998

The Journal of Experimental Medicine

208

161

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The transfer of lymphocytes into severe combined immunodeficiency (SCID) mice induces a series of histological changes in the spleen, including the appearance of mature follicular dendritic cells (FDCs). Studies were undertaken to clarify the role of lymphotoxin (LT) in this process. The results show that SCID mice have a small and partially differentiated white pulp containing marginal zone and interdigitating dendritic cells, but lacking FDCs. Transferred spleen cells can segregate into T and B cell areas shortly after their injection to SCID mice. This ability is dependent on signaling through LT-β receptor (LT-βR), since blocking ligand–receptor interaction in recipient SCID mice ablates the capacity of the transferred cells to segregate. A week after lymphocyte transfer, host-derived FDCs appeared in the reconstituted SCID mice. This induction of FDCs is dependent on LT-βR signaling by B cells since LT-α−/− B cells are incapable of inducing development of FDCs in SCID mice, even after cotransfer of LT-α+/+ T cells. Therefore, LT plays at least two discrete roles in splenic organization. First, it appears that LT induces the differentiation of the white pulp to create sites for lymphocyte segregation. Second, LT expression by B cells drives the maturation of FDCs and the organization of B cell follicles.

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Lymphotoxin gene expression by melanocytes and melanoma cell lines and persistence of unspliced mRNA

Cited by 8 publications

References 32 publications

The lymphotoxin β receptor is a potential therapeutic target in renal inflammation

The lymphotoxin β receptor is a potential therapeutic target in renal inflammation

Visualization of Lymphotoxin-β and Lymphotoxin-β Receptor Expression in Mouse Embryos

The Sequential Role of Lymphotoxin and B Cells in the Development of Splenic Follicles

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