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Platelet-Activating Factor Is Crucial In Psoralen And Ultraviolet A-Induced Immune Suppression, Inflammation, And Apoptosis., Peter Wolf, Dat X Nghiem, Jeffrey P Walterscheid, Scott Byrne, Yumi Matsumura, Yasuhiro Matsumura, Cora Bucana, Honnavara N Ananthaswamy, Stephen E Ullrich Sep 2006

Platelet-Activating Factor Is Crucial In Psoralen And Ultraviolet A-Induced Immune Suppression, Inflammation, And Apoptosis., Peter Wolf, Dat X Nghiem, Jeffrey P Walterscheid, Scott Byrne, Yumi Matsumura, Yasuhiro Matsumura, Cora Bucana, Honnavara N Ananthaswamy, Stephen E Ullrich

Journal Articles

Psoralen plus UVA (PUVA) is used as a very effective treatment modality for various diseases, including psoriasis and cutaneous T-cell lymphoma. PUVA-induced immune suppression and/or apoptosis are thought to be responsible for the therapeutic action. However, the molecular mechanisms by which PUVA acts are not well understood. We have previously identified platelet-activating factor (PAF), a potent phospholipid mediator, as a crucial substance triggering ultraviolet B radiation-induced immune suppression. In this study, we used PAF receptor knockout mice, a selective PAF receptor antagonist, a COX-2 inhibitor (presumably blocking downstream effects of PAF), and PAF-like molecules to test the role of PAF …


Implication Of A Retrovirus-Like Glycoprotein Peptide In The Immunopathogenesis Of Ebola And Marburg Viruses, Kavitha Yaddanapudi, Gustavo F. Palacios, Jonathan S. Towner, Ivy Chen, Carlos A. Sariol, Stuart T. Nichol, W. Ian Lipkin Jan 2006

Implication Of A Retrovirus-Like Glycoprotein Peptide In The Immunopathogenesis Of Ebola And Marburg Viruses, Kavitha Yaddanapudi, Gustavo F. Palacios, Jonathan S. Towner, Ivy Chen, Carlos A. Sariol, Stuart T. Nichol, W. Ian Lipkin

Public Health Resources

Ebola and Marburg viruses can cause hemorrhagic fever (HF) outbreaks with high mortality in primates. Whereas Marburg (MARV), Ebola Zaire (ZEBOV), and Ebola Sudan (SEBOV) viruses are pathogenic in humans, apes, and monkeys, Ebola Reston (REBOV) is pathogenic only in monkeys (1–3). Early immunosuppression may contribute to pathogenesis by facilitating viral replication (4–6). Lymphocyte depletion, intravascular apoptosis, and cytokine dysregulation are prominent in fatal cases (7). Here we functionally characterize a 17 amino acid domain in filoviral glycoproteins that resembles an immunosuppressive motif in retroviral envelope proteins (8, 9). Activated human or rhesus peripheral blood mononuclear cells (PBMC) were exposed …