RESUMO
The U.S. government has sought to restrict immigration under the "America First" doctrine. These policies severely harm American science by stripping it of talent and eliminating a major driver of its innovation engine. We urge scientists to work to reverse these policies and forcefully condemn anti-immigrant sentiments.
Assuntos
Ciência , COVID-19/epidemiologia , COVID-19/virologia , Emigrantes e Imigrantes , Emigração e Imigração , Humanos , Pessoal de Laboratório , SARS-CoV-2/fisiologia , Estados UnidosAssuntos
Alergia e Imunologia , Pessoas Famosas , Virologia , Animais , História do Século XX , Humanos , CamundongosAssuntos
Distinções e Prêmios , Pesquisa Biomédica/história , Neoplasias da Mama/imunologia , Linfócitos T Reguladores/imunologia , Neoplasias da Mama/patologia , Feminino , História do Século XX , História do Século XXI , Humanos , Masculino , Retratos como Assunto , Linfócitos T Reguladores/patologiaAssuntos
Linfócitos T CD4-Positivos/imunologia , Fator Regulador 1 de Interferon/fisiologia , Interferon gama/imunologia , Interleucina-12/fisiologia , Células Th1/imunologia , Animais , Linfócitos T CD4-Positivos/citologia , Diferenciação Celular , Fator Regulador 1 de Interferon/genética , Camundongos , Camundongos Knockout , Fator de Transcrição STAT4/fisiologia , Células Th1/citologiaAssuntos
Pesquisa Biomédica/história , Drosophila/fisiologia , Neurônios/fisiologia , Neurociências/história , Fisiologia/história , Animais , Distinções e Prêmios , História do Século XX , História do Século XXI , Humanos , Canais Iônicos/fisiologia , National Academy of Sciences, U.S. , Estados UnidosRESUMO
Two cytokine-inducible gene products, important in inflammation and infection, also play essential roles in female fertility. One of these is the product of tumor necrosis factor (TNF)-stimulated gene 6 (TSG-6), alternatively termed TNFAIP6 (for TNF-alpha-induced protein 6), originally cloned from diploid human fibroblasts stimulated with TNF. The second is pentraxin 3 (PTX3), also termed TSG-14, originally isolated from TNF-stimulated human fibroblasts and from interleukin-1 (IL-1)-stimulated vascular endothelial cells. TSG-6, which specifically binds to hyaluronan (HA) and to inter-alpha-inhibitor (I alpha I), shows potent anti-inflammatory activity in acute and chronic inflammation, notably in several models of autoimmune arthritis. PTX3 was shown to play an important role in resistance to fungal infection with Aspergillus fumigatus. Both TSG-6 and PTX3 are synthesized in the ovary prior to ovulation, where they become components of an expanding viscoelastic matrix that surrounds the oocyte before its release from the follicle at the ovarian surface. Female mice with a targeted disruption of either the TSG-6 or PTX3 gene show severe defects in fertility.
Assuntos
Proteína C-Reativa/genética , Moléculas de Adesão Celular/genética , Fertilidade/genética , Imunidade Inata , Componente Amiloide P Sérico/genética , alfa-Globulinas/metabolismo , Animais , Artrite Experimental/imunologia , Proteína C-Reativa/biossíntese , Moléculas de Adesão Celular/biossíntese , Condrócitos/metabolismo , Citocinas/fisiologia , Feminino , Fertilidade/imunologia , Expressão Gênica , Humanos , Ácido Hialurônico/metabolismo , Inflamação/imunologia , Oócitos/metabolismo , Ovário/metabolismo , Componente Amiloide P Sérico/biossínteseRESUMO
Cytokine research has spawned the introduction of new therapies that have revolutionized the treatment of many important diseases. These therapeutic advances have resulted from two very different strategies. The first therapeutic strategy embodies the administration of purified, recombinant cytokines. The second relies on the administration of therapeutics that inhibit the harmful effects of upregulated, endogenous cytokines. Examples of successful cytokine therapeutics include hematopoietic growth factors (colony stimulating factors) and interferons. Prime examples of cytokine antagonists that have profoundly altered the treatment of some inflammatory disorders are agents that inhibit the effects of tumor necrosis factor (TNF). In this article, we highlight some of the studies that have been responsible for the introduction of cytokine and anti-cytokine therapies, with emphasis on the development of interferons and anti-TNF agents.
Assuntos
Artrite Reumatoide/história , Citocinas/história , Interferons/história , Neoplasias/história , Artrite Reumatoide/tratamento farmacológico , Pesquisa Biomédica/história , Citocinas/antagonistas & inibidores , Citocinas/fisiologia , Citocinas/uso terapêutico , História do Século XX , Humanos , Interferons/genética , Interferons/uso terapêutico , Neoplasias/tratamento farmacológico , Ensaios Clínicos Controlados Aleatórios como Assunto/história , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Fator de Necrose Tumoral alfa/históriaRESUMO
Nearly half a century has passed since the first published description of interferons (IFNs). This commentary introduces the four accompanying review articles on type I IFN research and attempts to relate how the field of IFN research has been changing during its history.
Assuntos
Alergia e Imunologia/história , Interferons/história , Animais , História do Século XX , História do Século XXI , HumanosRESUMO
TNF-stimulated gene 6 (TSG-6) encodes a 35 kDa inducible secreted glycoprotein important in inflammation and female fertility. Previous studies have shown that TSG-6 has anti-inflammatory activity in models of acute and chronic inflammation. In the present study, we show that treatment of the RAW 264.7 murine macrophage cell line with TSG-6 protein up-regulates the expression of inducible cyclooxygenase-2 (COX-2), a key enzyme in inflammation and immune responses. This action of TSG-6 protein was abolished by heat denaturation, trypsin digestion, or anti-TSG-6 antibodies. TSG-6 treatment also resulted in a rapid increase in COX-2 mRNA levels, suggesting that TSG-6 up-regulates COX-2 gene expression. Up-regulation of COX-2 was accompanied by an increase in the production of prostaglandins, especially PGD2. As the PGD2 metabolite, 15-deoxy-Delta12,14-PGJ2, can act as a negative regulator of inflammation, these TSG-6 actions may explain, at least in part, the anti-inflammatory effect of TSG-6 observed in the intact organism.