scholarly journals Successful ultraviolet B treatment of psoriasis is accompanied by a reversal of keratinocyte pathology and by selective depletion of intraepidermal T cells.

1995 ◽  
Vol 182 (6) ◽  
pp. 2057-2068 ◽  
Author(s):  
J G Krueger ◽  
J T Wolfe ◽  
R T Nabeya ◽  
V P Vallat ◽  
P Gilleaudeau ◽  
...  
Keyword(s):  
T Cells ◽  
Granular Layer ◽  
Basal Layer ◽  
Ultraviolet B ◽  
Ki 67 ◽  
Keratin 16 ◽  
Selective Depletion ◽  
Skin Irradiation ◽  
Induced Apoptosis

Skin irradiation with ultraviolet B (UVB) is a common and often durable treatment for psoriasis and other inflammatory skin disorders. We studied the effects of UVB on keratinocytes and leukocytes in psoriatic tissue and in culture. In nine patients treated repetitively, most of the cellular and molecular changes that typify the psoriatic epidermis reverted to normal. Keratinocyte hyperplasia, assessed by expression of the Ki-67 cell cycle antigen, decreased by 70%, and residual cell proliferation was appropriately confined to the basal layer. Epidermal thickening was reduced by 60%, and a granular layer reformed. Expression of keratin 16, as well as suprabasal integrin alpha 3 and insulin-like growth factor-1 receptors, was eliminated, whereas filagrin increased markedly. UVB also depleted > 90% of the CD3+, CD8+, and CD25+ T cells from the psoriatic epidermis, whereas dermal T cells were only minimally depressed. The latter finding parallels the known inability of these doses of UVB to penetrate the dermis. In tissue culture, UVB was antiproliferative and cytotoxic toward T cells and keratinocytes, but the T cells were 10-fold more sensitive. Furthermore, low doses of UVB induced apoptosis in lymphocytes but not keratinocytes, as detected by the TUNEL (TdT-mediated dUTP-biotin nick end labeling) technique. The selective effects of UVB on intraepidermal T cells in situ and in culture support the hypothesis that epidermal alterations in psoriasis can be normalized by a depletion of activated intraepidermal T cells.

Primary Cutaneous Follicle Center Lymphoma in An HTLV-1 Carrier.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 5032-5032
Author(s):  
Adrienne A. Phillips ◽  
Zion Oshikanlu ◽  
Gerard J Nuovo ◽  
Govind Bhagat ◽  
David Savage
Keyword(s):  
T Cells ◽  
B Cell ◽  
Complete Blood Count ◽  
Conflicts Of Interest ◽  
B Cell Lymphoma ◽  
Excisional Biopsy ◽  
Good Health ◽  
Ki 67 ◽  
In Situ Pcr

Abstract Abstract 5032 Background Human T-lymphotropic virus type 1 (HTLV-1) is an oncogenic retrovirus associated with adult T-cell leukemia/lymphoma (ATLL), an aggressive neoplasm of mature CD4+ T-lymphocytes which always shows monoclonal integration of HTLV-1 provirus DNA. HTLV is not associated with B-cell non-Hodgkin's lymphoma (B-NHL); however rare cases of B-NHL have been reported in HTLV-1 carriers, leading some to hypothesize a role for HTLV-1 in B-cell lymphogenesis. We report a case of a Jamaican male HTLV-1 carrier with primary cutaneous follicle center lymphoma of B-cell origin and explore the link between HTLV-1 and B-NHL. Case Report A 55 year old Jamaican male was seen in our hematology clinic for evaluation of multiple scalp masses progressive over six months. The lesions were painful, pruritic, but not associated with other constitutional symptoms. He had been in good health prior to the onset of these symptoms, and denied toxic habits or exposures. Physical examination revealed multiple firm, non-tender scalp masses, the largest measuring 3.0 × 2.0 cm; the overlying skin was nodular and erythematous but without breakdown or discharge. His complete blood count, basic metabolic profile, hepatic function and lactate dehydrogenase were all within normal limits. On excisional biopsy, the dermis showed a dense lymphoid infiltrate of medium to large sized cells, with a nodular and trabecular pattern of growth from the superficial dermis to the aponeurosis. Numerous large centroblast-like cells were present. Immunohistochemical stains demonstrated the following phenotype: CD45+, CD20+, CD79a+, BCL2+/-, BCL6+/-, CD10+, and MUM-/+. A stain for CD21 highlighted compact and fused/contiguous follicular dendritic cell meshworks in association with the neoplastic B-cell infiltrate. Staining with Ki-67 highlighted a variable but high proliferation rate (80%). A moderate infiltrate of small-sized T-cells (CD3+, CD5+) was also present. These features were diagnostic of a primary cutaneous follicle center lymphoma. Evaluation with the MYC breakapart probe showed no evidence of rearrangement; RT in-situ PCR for HTLV-1 showed a signal in many of the infiltrating T-cells. He was seropositive for positive HTLV-1 and negative for HIV and EBV infection. Bone marrow biopsy and aspiration and additional staging CTs were unremarkable. The patient received 4 cycles of R-CHOP chemotherapy and has been in a complete remission for 2 years. Discussion We report a case of a Jamaican male HTLV-1 carrier with cutaneous lymphoma of B-cell origin with detection of HTLV-1 proviral DNA in the neoplastic cells by RT in-situ PCR. Our findings lead us to speculate that HTLV-1 infected T-cells and/or an immunodeficient state in certain HTLV-1 carriers might allow for the development of B-cell lymphoma. Further research on the pathogenesis of HTLV-1 in B cell lymphomagenesis needs to be explored. Disclosures No relevant conflicts of interest to declare.

Ultraviolet-B irradiation decreases IFN-γ and increases IL-4 expression in psoriatic lesional skin in situ and in cultured dermal T cells derived from these lesions

2003 ◽  
Vol 12 (2) ◽  
pp. 172-180 ◽  
Author(s):  
Gamze Piskin ◽  
Cornelis W. Koomen ◽  
Daisy Picavet ◽  
Jan D. Bos ◽  
Marcel B. M. Teunissen
Keyword(s):  
T Cells ◽  
Ultraviolet B ◽  
Lesional Skin ◽  
Ifn Γ ◽  
Ultraviolet B Irradiation

The Y-box binding protein YB-1 is associated with progressive disease and mediates survival and drug resistance in multiple myeloma

Blood ◽  
2008 ◽  
Vol 111 (7) ◽  
pp. 3714-3722 ◽  
Author(s):  
Manik Chatterjee ◽  
Christoph Rancso ◽  
Thorsten Stühmer ◽  
Niels Eckstein ◽  
Mindaugas Andrulis ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Drug Resistance ◽  
Disease Progression ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Binding Protein ◽  
Ki 67 ◽  
Induced Apoptosis

Abstract Current knowledge about molecular mechanisms underlying disease progression and drug resistance in multiple myeloma (MM) is still limited. Here, we analyzed the potential pathogenetic role of the Y-box binding protein YB-1 in MM. YB-1 is a member of the cold-shock domain protein superfamily and involved in various cellular functions such as proliferation. Immunohistochemical analyses revealed that neither normal bone marrow (BM) plasma cells (PCs), premalignant PCs of patients with monoclonal gammopathy of unknown significance (MGUS), nor MM cells with a mature morphology showed expression of YB-1 in situ. In contrast, YB-1 was strongly expressed in situ in normal PC precursor blasts as well as in a MM subset and in vitro in all of the evaluated MM cell lines. The YB-1–expressing MM cells were characterized by an immature morphology and a highly proliferative phenotype as defined by Ki 67 expression. We observed that siRNA-mediated knockdown of YB-1 decreased proliferation and induced apoptosis in MM cells even in the presence of BM stromal cells. Furthermore, we found that overexpression of YB-1 mediated resistance toward doxorubicin-induced apoptosis in MM cells. Thus, YB-1 contributes to disease progression, survival, and drug resistance in MM and might therefore provide an attractive therapeutic target.

The role of cbl family of ubiquitin ligases in gastric cancer exosome-induced apoptosis of Jurkat T cells

2009 ◽  
pp. 1-8
Author(s):  
Jing-Lei Qu ◽  
Xiu-Juan Qu ◽  
Ming-Fang Zhao ◽  
Yue-E Teng ◽  
Ye Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Ubiquitin Ligases ◽  
Jurkat T Cells ◽  
Induced Apoptosis

scholarly journals 5-ALA Attenuates the Palmitic Acid-Induced ER Stress and Apoptosis in Bovine Mammary Epithelial Cells

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1183
Author(s):  
Mst Mamuna Sharmin ◽  
Md Aminul Islam ◽  
Itsuki Yamamoto ◽  
Shin Taniguchi ◽  
Shinichi Yonekura
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Palmitic Acid ◽  
Er Stress ◽  
Aminolevulinic Acid ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Protective Effects ◽  
Bovine Mammary Epithelial Cells ◽  
Induced Apoptosis

The conservation of mammary gland physiology by maintaining the maximum number of mammary epithelial cells (MECs) is of the utmost importance for the optimum amount of milk production. In a state of negative energy balance, palmitic acid (PA) reduces the number of bovine MECs. However, there is no effective strategy against PA-induced apoptosis of MECs. In the present study, 5-aminolevulinic acid (5-ALA) was established as a remedial agent against PA-induced apoptosis of MAC-T cells (an established line of bovine MECs). In PA-treated cells, the apoptosis-related genes BCL2 and BAX were down- and upregulated, respectively. The elevated expression of major genes of the unfolded protein response (UPR), such as CHOP, a proapoptotic marker (C/EBP homologous protein), reduced the viability of PA-treated MAC-T cells. In contrast, 5-ALA pretreatment increased and decreased BCL2 and BAX expression, respectively. Moreover, cleaved caspase-3 protein expression was significantly reduced in the 5-ALA-pretreated group in comparison with the PA group. The downregulation of major UPR-related genes, including CHOP, extended the viability of MAC-T cells pretreated with 5-ALA and also reduced the enhanced intensity of the PA-induced expression of phospho-protein kinase R-like ER kinase. Moreover, the enhanced expression of HO-1 (antioxidant gene heme oxygenase) by 5-ALA reduced PA-induced oxidative stress (OxS). HO-1 is not only protective against OxS but also effective against ER stress. Collectively, these findings offer new insights into the protective effects of 5-ALA against PA-induced apoptosis of bovine MECs.

scholarly journals Expression of Semaphorin 3A in Malignant and Normal Bladder Tissue: Immunohistochemistry Staining and Morphometric Evaluation

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 109
Author(s):  
Ilan Bejar ◽  
Jacob Rubinstein ◽  
Jacob Bejar ◽  
Edmond Sabo ◽  
Hilla K Sheffer ◽  
...  
Keyword(s):  
Urothelial Carcinoma ◽  
Carcinoma In Situ ◽  
Urothelial Cancer ◽  
Basal Layer ◽  
Low Grade ◽  
High Grade ◽  
Bladder Tissue ◽  
Normal Bladder ◽  
Normal Bladder Tissue

Introduction: Our previous studies showed elevated levels of Semaphorin3a (Sema3A) in the urine of patients with urothelial cancer compared to healthy patients. The aim of this study was to analyze the extent of Sema3A expression in normal and malignant urothelial tissue using immune-staining microscopic and morphometric analysis. Materials and Methods: Fifty-seven paraffin-embedded bladder samples were retrieved from our pathology archive and analyzed: 14 samples of normal urothelium, 21 samples containing low-grade urothelial carcinoma, 13 samples of patients with high-grade urothelial carcinoma, 7 samples containing muscle invasive urothelial carcinoma, and 2 samples with pure urothelial carcinoma in situ. All samples were immunostained with anti Sema3A antibodies. The area of tissue stained with Sema3A and its intensity were analyzed using computerized morphometry and compared between the samples’ groups. Results: In normal bladder tissue, very light Sema3A staining was demonstrated on the mucosal basal layer and completely disappeared on the apical layer. In low-grade tumor samples, cells in the basal layer of the mucosa were also lightly stained with Sema3A, but Seama3A expression intensified upon moving apically, reaching its highest level on apical cells exfoliating to the urine. In high grade urothelial tumors, Seama3A staining was intense in the entire thickness of the mucosa. In samples containing carcinoma in situ, staining intensity was high and homogenous in all the neoplastic cells. Conclusions: Sema3A may be serve as a potential non-invasive marker of urothelial cancer.

Sign in / Sign up

Export Citation Format

Share Document