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287 results on '"Day, Noorbibi K."'

14. Pyogenic bacterial infections in humans with IRAK-4 deficiency. (Reports)

Author

Picard, Capucine, Puel, Anne, Bonnet, Marion, Ku, Cheng-Lung, Bustamante, Jacinta, Yang, Kun, Soudais, Claire, Dupuis, Stephanie, Feinberg, Jacqueline, Fieschi, Claire, Elbim, Carole, Hitchcock, Remi, Lammas, David, Davies, Graham, Ghonaium, Abdulaziz al-, Rayes, Hassan al-, Jumaah, Sulaiman al-, Hajjar, Sami al-, Mohsen, Ibrahim Zaid al-, Frayha, Husn H., Rucker, Rajivi, Hawn, Thomas R., Aderem, Alan, Tufenkeji, Haysam, Haraguchi, Soichi, Day, Noorbibi K., Good, Robert A., Gougerot-Pocidalo, Marie-Anne, Ozinsky, Adrian, and Casanova, Jean-Laurent

Subjects
Children -- Diseases -- Research, Immunity -- Research, Gram-positive bacterial infections -- Prevention -- Research, Interleukin-1 -- Research, Science and technology, Diseases, Prevention, Research
Abstract

Members of the Toll-like receptor (TIR) and interleukin-1 receptor (IL-1R) superfamily share an intracytoplasmic Toll-IL-1 receptor (TIR) domain, which mediates recruitment of the interleukin-1 receptor-associated kinase (IRAK) complex via TIR-containing adapter molecules. We describe three unrelated children with inherited IRAK-4 deficiency. Their blood and fibroblast cells did not activate nuclear factor KB and mitogen-activated protein kinase (MAPK) and failed to induce downstream cytokines in response to any of the known ligands of TIR-bearing receptors. The otherwise healthy children developed infections caused by pyogenic bacteria. These findings suggest that, in humans, the TIR-IRAK signaling pathway is crucial for protective immunity against specific bacteria but is redundant against most other microorganisms., The members of the mammalian Toll-like/ interleukin-1 receptor superfamily characteristically have a TIR domain (1). This superfamily contains two classes of membrane receptors: TLRs, seven of which recognize known ligands [...]

Published
2003

15. IRAK-4- and MyD88-Dependent Pathways Are Essential for the Removal of Developing Autoreactive B Cells in Humans

Author

Isnardi, Isabelle, Ng, Yen-Shing, Srdanovic, Iva, Motaghedi, Roja, Rudchenko, Sergei, von Bernuth, Horst, Zhang, Shen-Ying, Puel, Anne, Jouanguy, Emmanuelle, Picard, Capucine, Garty, Ben-Zion, Camcioglu, Yildiz, Doffinger, Rainer, Kumararatne, Dinakantha, Davies, Graham, Gallin, John I., Haraguchi, Soichi, Day, Noorbibi K., Casanova, Jean-Laurent, and Meffre, Eric

Published
2008
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31. Complement in Cancer

Author

Kassel, Robert L., Hardy, William D., Jr., Day, Noorbibi K., Good, Robert A., editor, Day, Stacey B., editor, and Day, Noorbibi K., editor

Published
1977
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35. LMP-420, a small-molecule inhibitor of TNF-alpha, reduces replication of HIV-1 and Mycobacterium tuberculosis in human cells

Author

Tangsinmankong Nutthapong, Stenger Steffen, Beigier-Pompadre Macarena, Kamchaisatian Wasu, Day Noorbibi K, Haraguchi Soichi, Sleasman John W, Pizzo Salvatore V, and Cianciolo George J

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Co-infections of human immunodeficiency virus (HIV) and Mycobacterium tuberculosis (M. Tb) are steadily increasing and represent a major health crisis in many developing countries. Both pathogens individually stimulate tumor necrosis factor-alpha (TNF) release from infected cells and TNF, in turn, enhances the replication of each. A recent report on a Phase I clinical trial suggested that etanercept (soluble TNF receptor) might be beneficial in treating HIV/M. Tb co-infected patients. We sought to determine if a small molecule inhibitor of TNF synthesis and activity could block replication of either organism and thus be a potential adjunct to existing drugs targeting these agents. Results LMP-420, a novel anti-inflammatory agent that inhibits TNF, was tested for HIV-1 inhibition both alone and in combination with AZT (3' -azido-3-deoxythymidine). LMP-420 alone was tested against M. Tb. HIV-1 infected human peripheral blood mononuclear cells (PBMC) or M. Tb-infected human alveolar macrophages (AM) were treated with a single dose of LMP-420 and viral or bacterial replication determined after 7 or 5 days respectively. Viral replication was determined from supernatant p24 levels measured by ELISA. M. Tb replication was determined by bacterial culture of macrophage lysates. LMP-420 alone inhibited HIV replication over 7 days with an IC50 of ~300 nM. Combination of LMP-420 with AZT doubled the level of HIV inhibition observed with AZT alone. LMP-420 alone inhibited the replication of virulent M. Tb by >80%, more than that observed with anti-TNF antibody alone. Conclusion Inhibition of TNF with inexpensive, small-molecule, orally-active drugs may represent a useful strategy for enhancing the activity of currently-available antiviral and anti-M. Tb agents, particularly in those areas where co-infections with these pathogens act to synergistically enhance each other.

Published
2006
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37. Alteration of in vivo cytokine gene expression in mice infected with a molecular clone of the defective MAIDS virus

Author

Bradley, W. Guy, Ogata, Nahoko, Good, Robert A., and Day, Noorbibi K.

Subjects
Cytokines -- Genetic aspects, CD4 lymphocytes -- Physiological aspects, HIV (Viruses) -- Physiological aspects, Mice -- Diseases, Health
Abstract

The defective murine acquired immunodeficiency syndrome (MAIDS) virus may affect the production of cytokines in mice. Cytokines are protein released by one cell population after contact with an antigen to mediate immune response. The development and progression of MAIDS is used as a model of HIV infection in humans. Researchers examined the effect of the defective MAIDS virus on cytokine production in mice. Infection with defective MAIDS virus was associated with changes in cytokine production. This change was accompanied by a rise in spleen cell levels, higher production of immunoglobulin M and increased replication of the defective MAIDS virus. HIV may affect the immune system of humans in a similar manner.

Published
1994

41. Pediatric AIDS with severe T-cell depression and hypogammaglobulinemia

Author

Koutsonikolis, Angelos, Nelson, Robert P., Jr., Kornfeld, Stephen J., Day, Noorbibi K., and Good, Robert A.

Subjects
AIDS (Disease) in children -- Physiological aspects, Gamma globulins -- Physiological aspects, Health
Abstract

Some children infected with HIV may present with low blood levels of gammaglobulins. A 10-month-old girl was admitted with a respiratory infection that was diagnosed as Pneumoncystis carinii pneumonia. She had markedly low levels of T-cells and gammaglobulin. She had a positive ELISA test for HIV but a negative polymerase chain reaction test (PCR), a test that amplifies amounts of viral DNA in the blood to detectable levels. HIV cultures were positive. Her mother's ELISA was positive, although the parents denied intravenous drug use, and an HIV test in the first trimester of pregnancy was negative. The child died of respiratory failure. The usual presentation with HIV infection is high levels of gammaglobulin because the virus activates B lymphocytes. However, about 2% of cases will present with low gammaglobulin. The false-negative PCR may be due to the extremely low numbers of T-cells yielding insufficient viral particles.

Published
1995

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