scholarly journals Cumulative exposure to solar ultraviolet A & B increases apoptosis of peripheral blood cutaneous lymphocyte antigen (CLA)+ T-Lymphocytes in outdoor workers

Author(s):  
Afif Nurul Hidayati ◽  
Saut Sahat Pohan ◽  
Widodo J. Pudjirahardjo ◽  
Isaak Effendy
1996 ◽  
Vol 39 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Costantino Pitzalis ◽  
Alberto Cauli ◽  
Nicolo Pipitone ◽  
Catherine Smith ◽  
Jonathan Barker ◽  
...  

1994 ◽  
Vol 127 (5) ◽  
pp. 1485-1495 ◽  
Author(s):  
R Alon ◽  
H Rossiter ◽  
X Wang ◽  
T A Springer ◽  
T S Kupper

Memory T lymphocytes extravasate at sites of inflammation, but the mechanisms employed by these cells to initiate contact and tethering with endothelium are incompletely understood. An important part of leukocyte extravasation is the initiation of rolling adhesions on endothelial selectins; such events have been studied in monocytes and neutrophils but not lymphocytes. In this study, the potential of T lymphocytes to adhere and roll on endothelial selectins in vitro was investigated. We demonstrate that T cells can form tethers and rolling adhesions on P selectin and E selectin under physiologic flow conditions. Tethering and rolling on P selectin was independent of cell-surface cutaneous lymphocyte antigen (CLA) expression, which correlated strictly with the capacity of T cells to form rolling adhesions under flow on E selectin. T cell tethering to P selectin was abolished by selective removal of cell surface sialomucins by a P. haemolytica O-glycoprotease, while cutaneous lymphocyte antigen expression was unaffected. A sialomucin molecule identical or closely related to P selectin glycoprotein ligand-1 (PSGL-1), the major P selectin ligand on neutrophils and HL-60 cells, appears to be a major T cell ligand for P selectin. P selectin glycoprotein ligand-1 does not appear to support T cell rolling on E selectin. In turn, E selectin ligands do not appear to be associated with sialomucins. These data demonstrate the presence of structurally distinct ligands for P or E selectins on T cells, provide evidence that both ligands can be coexpressed on a single T cell, and mediate tethering and rolling on the respective selectins in a mutually exclusive fashion.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1785-1785
Author(s):  
Dorna Rezania ◽  
Elizabeth Sagatys ◽  
L. Frank Glass ◽  
Marshall E. Kadin ◽  
Hernani Cualing

Abstract Lymphomatoid papulosis (LyP) and primary cutaneous anaplastic large cell lymphoma (pcALCL) comprise a spectrum of CD30+ lymphoproliferative disease with overlapping morphology and clinical behavior. The border between LyP and ALCL is often difficult to establish. Moreover, secondary skin lesions of systemic ALCL closely resemble pcALCL and confer a poor prognosis. Thus, it is important to develop new criteria to make these distinctions. This study uses tumor necrosis factor receptor (TNFR)-associated factor 1 (TRAF-1) and cutaneous lymphocyte antigen (CLA) in differentiating CD30-positive lymphoproliferations involving the skin. TRAF-1 is involved in the intracellular signal transduction of TNFR family members without a death domain. TRAF-1 is expressed mainly in activated lymphocytes and strongly induced by NF-kB. CLA is an E-selectin ligand that facilitates adhesion of T lymphocytes to cutaneous vascular endothelium, initiating egress of T lymphocytes to the skin from the systemic circulation. After obtaining SRC and IRB approval, formalin-fixed, paraffin-embedded biopsy specimens from confirmed cutaneous and systemic CD30+ lymphomas were selected from the pathology department of Moffitt Cancer database, 2000–2007. The selected cases included 13 LyP, 9 primary cutaneous ALCL, and 8 systemic ALCL. All cases were stained with TRAF-1 (Imgenex IMG 5757) and CLA (HECA 452) using manufacturer’s protocols. Manual morphometry of 500 lymphocytes counted under high power view (40x HPF) and virtual flow cytometry were performed to quantitate the degree of antibody expression. Antigen expression was scored as negative (less than 5%), weak positive (5 to 50%), intermediate positive (50–80%) and strong positive (80–100%). TRAF-1 was expressed by > 5% of CD30+ large atypical cells in 12 out of 13 LyP cases and in all nine pcALCL. TRAF-1 expression was virtually absent in systemic ALCL with or without skin manifestations. There was no significant difference of TRAF-1 staining between LyP and pcALCL (p>0.05), but significant significant differences betweeen LyP and systemic ALCL (p<0.01), and between pcALCL vs systemic ALCL (p <0.001). Tumor cells of all cases of systemic ALCL case were negative for TRAF-1 (p= 0.0003). CLA expression showed significant differences between LyP and pcALCL (p<0.05) as well as LyP and systemic ALCL (p<0.001), and insignificant differences between pcALCL and systemic ALCL( p>0.05). Mean expression of TRAF-1 was 25% in LyP vs 32% in pcALCL and 0.87% in systemic ALCL. CLA had a mean of 52% for LyP, 28.5% for pcALCL and 6.5% for systemic ALCL. In conclusion, (1) there is significant differential expression of TRAF-1 and CLA in LyP, (2) pcALCL and systemic ALCL. CLA can differentiate LyP from pcALCL. Strong TRAF-1 expression is almost restricted to CD30+ cells in LyP and intermediate to high expression in primary cutaneous ALCL. Systemic ALCL is uniformly negative for TRAF-1. This study indicates potential utility of TRAF-1 and CLA expression data in separating systemic from pcCD30-positive lymphoproliferative disorders.


1999 ◽  
Vol 197 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Tadashi Yoshino ◽  
Mitsuhiro Okano ◽  
Hong-Li Chen ◽  
Junjiro Tsuchiyama ◽  
Eisaku Kondo ◽  
...  

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yixuan Liu ◽  
Suhong Xie ◽  
Lei Li ◽  
Yanhui Si ◽  
Weiwei Zhang ◽  
...  

Abstract Background This study investigates the effect of autologous bone marrow transfusion (BMT) on the reconstruction of both bone marrow and the immune system in patients with AIDS-related lymphoma (ARL). Methods A total of 32 patients with ARL participated in this study. Among them, 16 participants were treated with conventional surgery and chemotherapy (control group) and the remaining 16 patients were treated with chemotherapy followed by autologous bone marrow transfusion via a mesenteric vein (8 patients, ABM-MVI group) or a peripheral vein (8 patients, ABM-PI group). Subsequently, peripheral blood and lymphocyte data subsets were detected and documented in all patients. Results Before chemotherapy, no significant difference in indicators was observed between three groups of ARL patients. Unexpectedly, 2 weeks after the end of 6 courses of chemotherapy, the ABM-MVI group, and the ABM-PI group yielded an increased level of CD8+T lymphocytes, white blood cells (WBC), and platelet (PLT) in peripheral blood in comparison to the control group. Notably, the number of CD4+T lymphocytes in the ABM-PI group was significantly higher than that in the other two groups. Additionally, no significant difference in haemoglobin levels was observed before and after chemotherapy in both the ABM-MVI and ABM-PI groups, while haemoglobin levels in the control group decreased significantly following chemotherapy. Conclusions Autologous bone marrow transfusion after chemotherapy can promote the reconstruction of both bone marrow and the immune system. There was no significant difference in bone marrow recovery and reconstruction between the mesenteric vein transfusion group and the peripheral vein transfusion group.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 578.1-579
Author(s):  
S. Schnitte ◽  
A. Fuchs ◽  
T. Funk ◽  
A. C. Pecher ◽  
D. Dörfel ◽  
...  

Background:Psoriasis is a frequent skin disease that can appear with an arthritic manifestation in approximately 30% of the cases [1]. The underlying excessive immune reaction caused by pro-inflammatory cytokines can be triggered by several risk factors [2]. Various subgroups of Dendritic cells (DCs) in the skin play a crucial role in the induction of the dermal inflammatory response [3].Objectives:As the role of peripheral blood DCs remains unknown and the cause of an arthritic manifestation is still not completely understood [4], this project aimed to detect differences in phenotype or function of peripheral blood DCs in psoriatic patients with or without arthritis.Methods:We analyzed peripheral blood cells of 60 psoriasis patients with and without arthritis. Different DC subpopulations were detected by flow cytometry. Monocyte-derived DCs were cultured with or without Lipopolysaccharides to gain immature (iDC) and mature (mDC) cells. The DC phenotype was determined by staining with CD80, CD83, CD86, CD206, CCR7, CD1a, HLA-DR, CD40, GPN-MB, DC209 and CD14. Their T-cell stimulatory capability was analyzed by co-incubation with Carboxyfluorescein succinimidyl ester stained lymphocytes and the quantification of CD4+ T-lymphocytes afterwards. To measure the migration capacity DCs were seated into transwell chambers with a semipermeable membrane and partly supplemented with Macrophage Inflammatory Protein 3 Beta (Mip3b). Migrated cells were detected by flow cytometry. Measured cell counts were normalized to cell counts without Mip3b stimulation.Results:Comparing the factor of increase of migrated mDC counts due to mip3b stimulation, we detected a significant lower rate in samples of patients with arthritis (PsA) compared to those of patients without (Ps). Assays of mDCs without mip3b stimulation showed a significant higher count of migrated cells in the samples of the arthritic group [Figure 1]. Cell counts with Mip3b stimulation did vary slightly in the groups. The DC subpopulations and the expression of analyzed cell surface proteins did not show significant differences. The amounts of stimulated T-Lymphocytes did not differ significantly.Figure 1.Migration essay showing mDCs following Mip3b (+miß3b) as multiples of mDCs without stimulation (-mip3b). The factor of increase is significantly lower in patients with arthritis (PsA) compared to patients without (Ps). Absolute counts of migrated mDCs without Mip3b are significantly higher in the arthritic group. Cell counts with stimulation do not differ significantly (data not shown). N=24, p<0.05Conclusion:CCL19 (Mip3b) is a potent ligand to the CCR7 receptor inducing migration of DCs towards the lymphatic node [5]. The CCR7 amounts on the DC surface did not differ significantly in the groups. The mDCs without CCL19 stimulation migrated in higher amounts in samples of arthritic patients. Cell counts of stimulated DCs showed only slight differences. These results could be generated by a different appearance of the DCs of arthritic patients that might facilitate migration. Further experiments focusing on this aspect should be performed. A possible effect of disruptive factors (age, sex, medication…) needs to be clarified.References:[1]Henes, J.C., et al.,High prevalence of psoriatic arthritis in dermatological patients with psoriasis: a cross-sectional study.Rheumatol Int, 2014.34(2): p. 227-34.[2]Lee, E.B., et al.,Psoriasis risk factors and triggers.Cutis, 2018.102(5s): p. 18-20.[3]Kim, T.G., S.H. Kim, and M.G. Lee,The Origin of Skin Dendritic Cell Network and Its Role in Psoriasis.Int J Mol Sci, 2017.19(1).[4]Veale, D.J. and U. Fearon,The pathogenesis of psoriatic arthritis.Lancet, 2018.391(10136): p. 2273-2284.[5]Ricart, B.G., et al.,Dendritic cells distinguish individual chemokine signals through CCR7 and CXCR4.J Immunol, 2011.186(1): p. 53-61.Acknowledgments:This project was financially supported by Novartis Pharma GmbH.Disclosure of Interests:Sarah Schnitte Grant/research support from: Reaserch grant by Novartis, Alexander Fuchs: None declared, Tanja Funk: None declared, Ann-Christin Pecher: None declared, Daniela Dörfel: None declared, Jörg Henes Grant/research support from: Novartis, Roche-Chugai, Consultant of: Novartis, Roche, Celgene, Pfizer, Abbvie, Sanofi, Boehringer-Ingelheim,


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