Tamara Loos
149587969
Respectability's edge: Transnational sex radical Rene Guyon
The writings and life of French sex radical, Rene Guyon (1876 1963) offer a fascinating opportunity to examine together western European sexological thought, human rights movements, and imperial privilege in Asia. As one of France's early promoters of sexual rights as a human right, Guyon revealed himself to be a radical advocate for sexual liberation from what he called the 'hideous bondage of conventional "sexual morality" in Europe and America. From his residence in Siam, Guyon penned his magnum opus, Etudes d'ethiques sexueles, a series of nine volumes that he wrote between 1929 and 1944 in which he promoted all consensual sexual acts, regardless of one's sex, age or race, within 'ethical limitations. His law background earned him a high position in the Ministry of Justice in Siam, where he worked as a legal reformer and judge from 1908 until 1963. His 50 plus years of experience in Siam and sexual adventures in other non western countries served as an unacknowledged springboard for his views and provided him invaluable credentials in the eyes of his western sexologist peers. I examine the relationships among his excoriation of western sexual mores, his concept of a sexual utopia, and his life experiences in Africa, Asia and other non western areas of the world. An examination of the life of one of France's first promoters of sexual rights reveals the fissures within nascent human rights movements in Europe and reflects on the implications of his peculiar defense of the non western countries where he worked.
Tamara Loos
229291221
Reading Gender Trouble in Southeast Asia
Judith Butler's book Gender Trouble, published in 1990, enjoyed its thirtieth anniversary in 2020. To that end, the Association for Asian Studies, the United States' largest association of academics working on Asia, invited scholars to consider the importance of her arguments and ideas for Asian studies and scholarship in Asia, including how scholars have diverged from and expanded their studies of gender and sexuality in ways not anticipated by Butler when she first published the book. In this essay, I examine the impact of Butler's book in Southeast Asia. Out of the abundance of scholarship stemming from and about the region's eleven diverse countries and their histories, I prioritize those works that explicitly engage the theoretical insights in Gender Trouble to elucidate the lives of gender nonconforming communities in Southeast Asia. I include scholarship that allows me to explore the disjunction between categories of analysis that are foundational to Butler's theory and those at work in Southeast Asia. Far from rendering Butler's theory and methodological intervention inapposite, this mismatch has catalyzed productive rethinking of Gender Trouble and its implications for the region.
The Journal of Asian Studies
Tamara Loos
198557039
CHAPTER THREE. RENEGADE ROYALIST: AUTOBIOGRAPHY AND SIAM'S DISAVOWED PRINCE PRISDANG
Tamara Loos
167119690
Deploying Theravada Buddhist Geographies in the Age of Imperialism
Asia Inside Out
Tamara Loos
23548518
Citrullination of CXCL10 and CXCL11 by peptidylarginine deiminase: a naturally occurring posttranslational modification of chemokines and new dimension of immunoregulation.
Interactions between chemokines and enzymes are vital in immunoregulation. Structural protein citrullination by peptidylarginine deiminase (PAD) has been associated with autoimmunity. In this report, we identified a novel naturally occurring posttranslational modification of chemokines, that is, the deimination of arginine at position 5 into citrulline of CXC chemokine ligand 10 (CXCL10) by rabbit PAD and human PAD2. Citrullination reduced 10 fold) the chemoattracting and signaling capacity of CXCL10 for CXC chemokine receptor 3 (CXCR3) transfectants; however, it did not affect CXCR3 binding. On T lymphocytes, though, citrullinated CXCL10 remained active but was again weaker than authentic CXCL10. PAD was also able to convert CXCL11, causing an impairment of CXCR3 signaling and T cell activation, though less pronounced than for CXCL10. Similarly, receptor binding properties of CXCL11 were not altered by citrullination. However, deimination decreased heparin binding properties of both CXCL10 and CXCL11. Overall, chemokines are the first immune modulators reported of being functionally modified by citrullination. These data provide new structure function dimensions for chemokines in leukocyte mobilization, disclosing an anti inflammatory role for PAD. Additionally because citrullination has severe consequences for chemokine biology, this invites to reassess the involvement and impact of PAD and citrullinated peptides in inflammation, autoimmunity, and hematologic disorders.
Blood
Tamara Loos Anneleen Viona Mortier Mieke Gouwy Isabelle Ronsse Willy Put Jan Lenaerts Jo Van Damme Paul Proost
14529848
Citrullination of CXCL8 by peptidylarginine deiminase alters receptor usage, prevents proteolysis, and dampens tissue inflammation
Biological functions of proteins are influenced by posttranslational modifications such as on/off switching by phosphorylation and modulation by glycosylation. Proteolytic processing regulates cytokine and chemokine activities. In this study, we report that natural posttranslational citrullination or deimination alters the biological activities of the neutrophil chemoattractant and angiogenic cytokine CXCL8/interleukin 8 (IL 8) Citrullination of arginine in position 5 was discovered on 14% of natural leukocyte derived CXCL8(1 77) generating CXCL8(1 77)Cit5. Peptidylarginine deiminase (PAD) is known to citrullinate structural proteins, and it may initiate autoimmune diseases. PAD efficiently and site specifically citrullinated CXCL5, CXCL8, CCL17, CCL26, but not IL 1b. In comparison with CXCL8(1 77) CXCL8(1 77)Cit5 had reduced affinity for glycosaminoglycans and induced less CXCR2 dependent calcium signaling and extracellular signal regulated kinase 1/2 phosphorylation. In contrast to CXCL8(1 77) CXCL8(1 77)Cit5 was resistant to thrombin or plasmin dependent potentiation into CXCL8(6 77) Upon intraperitoneal injection, CXCL8(6 77) was a more potent inducer of neutrophil extravasation compared with CXCL8(1 77) Despite its retained chemotactic activity in vitro, CXCL8(1 77)Cit5 was unable to attract neutrophils to the peritoneum. Finally, in the rabbit cornea angiogenesis assay, the equally potent CXCL8(1 77) and CXCL8(1 77)Cit5 were less efficient angiogenic molecules than CXCL8(6 77) This study shows that PAD citrullinates the chemokine CXCL8, and thus may dampen neutrophil extravasation during acute or chronic inflammation.
The Journal of experimental medicine
Paul Proost Tamara Loos Anneleen Viona Mortier Evemie Schutyser Mieke Gouwy Sam Noppen Chris Dillen Isabelle Ronsse Rene Conings Sofie Struyf Ghislain Opdenakker Prabhat C Maudgal Jo Van Damme
3701768
Improved planning of leukapheresis endpoint with customized prediction algorithm: minimizing collection days, volume of blood processed, procedure time, and citrate toxicity
Increased emphasis on cost and productivity in apheresis centers calls for a proficient and predictable hematopoietic progenitor cell (HPC) collection. Therefore, the aim of this study was to determine the value of a customized predictive algorithm that estimates how many blood volumes are required to process for a targeted CD34 cell dose.
Transfusion
Daniel L Leberfinger Kira L Badman Joseph M Roig Tamara Loos
37485809
TLR ligands and cytokines induce CXCR3 ligands in endothelial cells: enhanced CXCL9 in autoimmune arthritis
CXC chemokines are potent attractants of neutrophil granulocytes, T cells or natural killer cells. Toll like receptors (TLR) recognize microbial components and are also activated by endogenous molecules possibly implicated in autoimmune arthritis. In contrast to CXC chemokine ligand 8 (CXCL8) no CXC chemokine receptor 3 (CXCR3) ligand (ie CXCL9, CXCL10 and CXCL11) was induced by bacterial TLR ligands in human microvascular endothelial cells (HMVEC) However, peptidoglycan (PGN) double stranded (ds) RNA or lipopolysaccharide (LPS) (TLR2, TLR3 or TLR4 ligands, respectively) synergized with interferon g (IFN g) at inducing CXCL9 and CXCL10. In contrast, enhanced CXCL11 secretion was only obtained when IFN g was combined with TLR3 ligand. Furthermore, flagellin, loxoribine and unmethylated CpG oligonucleotide (TLR5, TLR7 and TLR9 ligands, respectively) did not enhance IFN g dependent CXCR3 ligand production in HMVEC. In analogy with TLR ligands, tumor necrosis factor a (TNF a) or interleukin 1b (IL 1b) in combination with IFN g, synergistically induced CXCL9 and CXCL11 in HMVEC and human fibroblasts, two fundamental cell types delineating the joint cavity. Etanercept, a humanized soluble recombinant p75 TNF receptor/IgG1Fc fusionprotein, neutralized synergistic CXCL9 production induced by TNF a plus IFN g, but not synergy between IFN g and the TLR ligands PGN or LPS. Synovial chemokine concentrations exemplify the fysiopathological relevance of the observed in vitro chemokine production patterns. In synovial fluids of patients with spondylarthropathies (ie ankylosing spondylitis or psoriatic arthritis) or rheumatoid arthritis, significantly enhanced CXCL9, but not CXCL11 levels, were detected compared to concentrations in synovial fluids of patients with metabolic crystal induced arthritis. Thus, CXCL9 is an important chemokine in autoimmune arthritis.
Laboratory Investigation
Tamara Loos Lies Dekeyzer Sofie Struyf Evemie Schutyser Klara Gijsbers Mieke Gouwy Annelies Fraeyman Willy Put Isabelle Ronsse Bernard A M Grillet Ghislain Opdenakker Jo van Damme Paul Proost
2164029
Proteolytic processing of CXCL11 by CD13/aminopeptidase N impairs CXCR3 and CXCR7 binding and signaling and reduces lymphocyte and endothelial cell migration.
CXCR3 ligands were secreted by tissue fibroblasts and peripheral blood derived mononuclear leukocytes in response to interferon gamma (IFN gamma) and Toll like receptor (TLR) ligands. Subsequent purification and identification revealed the presence of truncated CXCL11 variants missing up to 6 amino acids. In combination with CD26/dipeptidyl peptidase IV, the metalloprotease aminopeptidase N (APN) identical to the myeloid cell marker CD13, rapidly processed CXCL11, but not CXCL8, to generate truncated CXCL11 forms. Truncated CXCL11 had reduced binding, signaling, and chemotactic properties for lymphocytes and CXCR3 or CXCR7 transfected cells. CD13/APN truncated CXCL11 failed to induce an intracellular calcium increase but was still able to bind and desensitize CXCR3 for intact CXCL11 signaling. CXCL11 efficiently bound to CXCR7, but CXCL11 was not able to induce calcium signaling or ERK1/2 or Akt phosphorylation through CXCR7. CD26 truncated CXCL11 failed to attract lymphocytes but still inhibited microvascular endothelial cell (HMVEC) migration. However, further processing of CXCL11 by CD13 resulted in significant reduction of inhibition of HMVEC migration. Taken together, during inflammation or cancer, CXCL11 processing by CD13 may lead to a reduced number of tumor infiltrating lymphocytes and in a more angiogenic environment.
Blood
Paul Proost Anneleen Viona Mortier Tamara Loos Jo Vandercappellen Mieke Gouwy Isabelle Ronsse Evemie Schutyser Willy Put Marc Parmentier Sofie Struyf Jo Van Damme
205176884
Epidermal Expression and Regulation of Interleukin 33 during Homeostasis and Inflammation: Strong Species Differences.
IL 33 is a novel IL 1 family member with a putative role in inflammatory skin disorders and a complex biology. Therefore, recent conflicting data regarding its function in experimental models justify a close assessment of its tissue expression and regulation. Indeed, we report here that there are strong species differences in the expression and regulation of epidermal IL 33. In murine epidermis, IL 33 behaved similar to an alarmin, being constitutively expressed in keratinocyte nuclei and rapidly lost during acute inflammation. By contrast, human and porcine IL 33 were weakly expressed or absent in keratinocytes of noninflamed skin but induced during acute inflammation. To this end, we observed that expression of IL 33 in human keratinocytes but not murine keratinocytes was strongly induced by IFN g, and this upregulation completely depended on the presence of EGFR ligands. Accordingly, IFN g increased the expression of IL 33 in the basal layers of the epidermis in human ex vivo skin cultures only, despite good evidence of IFN g activity in cultures from both species. Together these findings demonstrate that a full understanding of IL 33 function in clinical settings must take species specific differences into account.
The Journal of investigative dermatology
Olav Sundnes Wojciech Pietka Tamara Loos Jon Sponheim Andrew L Rankin Stefan Pflanz Vibeke Bertelsen Jan Cezary Sitek Johanna Hol Guttorm Haraldsen Denis Khnykin