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7. Genetic variability in HIV-1 gp120 affects interactions with HLA molecules and T cell receptor

Author

Callahan, Kevin M., Fort, Madeline M., Obah, Eugene A., Reinherz, Ellis L., and Siliciano, Robert F.

Subjects
HLA histocompatibility antigens -- Physiological aspects, HIV (Viruses) -- Genetic aspects, Virus-induced immunosuppression -- Genetic aspects, Cellular immunity -- Genetic aspects, T cells -- Physiological aspects, Health
Abstract

The envelope protein gp120, part of the outer layer of the human immunodeficiency virus (HIV), can be different in various strains of the virus. Differences can occur within strains isolated from separate individuals and can even occur within different isolates from the same individual. Understanding the genetic variability is important as the gp120 protein is involved in cell-mediated immunity against HIV-infected cells, and this variability has allowed the virus to evade immune responses by the individual. The envelope protein gp120 has been the prime target in vaccine development, but its genetic variability has complicated this research. The envelope protein of the virus is processed and forms a complex with molecules known as the major histocompatibility complex (MHC). The complex then binds to a molecule, known as CD4, on T helper cells and other cells of the immune system, which stimulate the production of an immune response. Peptides (portions of proteins) of the gp120 molecule from different isolates were tested for their ability to stimulate helper T cells. If the peptides did not cause immune stimulation, the reason could be that the peptides could not form a complex with the MHC molecule, or they could form a complex, but the complex could not bind to the CD4 molecule on helper T cells. Peptides to the gp120 molecule in 12 of 14 strains tested could bind to the MHC molecule. However, in two strains, the variability in the gp120 molecules prevented the initial interaction between the gp120 and the MHC molecules. These strains were obtained from Africa and were highly divergent from the North American strains. Most of the variations still allowed the peptide to form a complex with the MHC. Therefore, many individuals can respond to a variety of gp120 molecules. In some strains, the peptide/MHC complex could be formed, but the complex could not interact with helper T cells. This indicates that, although the genetic variants of gp120 may be able to evade ongoing T cell responses, new responses will be generated. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

8. Lessons From Genetically Engineered Animal Models XII. IL-10-deficient (IL-[10.sup.-/-]) mice and intestinal inflammation

Author

RENNICK, DONNA M. and FORT, MADELINE M.

Subjects
Interleukin-10 -- Physiological aspects, Intestines -- Inflammation, Biological sciences
Abstract

Rennick, Donna M., and Madeline M. Fort. Lessons From Genetically Engineered Animal Models. XII. IL-10-deficient (IL-[10.sup.-/-]) mice and intestinal inflammation. Am J Physiol Gastrointest Liver Physiol 278: G829-G833, 2000. --Interleukin (IL)-[10.sup.-/-] mice spontaneously develop intestinal inflammation characterized by discontinuous transmural lesions affecting the small and large intestine and by dysregulated production of proinflammatory cytokines. The uncontrolled generation of IFN-[Gamma]-producing [CD4.sup.+] T cells (Th1 type) has been shown to play a causal role in the development of enterocolitis affecting these mutants. This article discusses studies of IL-[10.sup.-/-] mice that have investigated the role of enteric organisms in triggering intestinal disease, the mediators responsible for initiating and maintaining intestinal disease, the role IL-10 plays in the generation and/or function of regulatory cells, and the results of IL-10 therapy in experimental animal models of inflammatory bowel disease (IBD) and human patients with IBD. interleukin; counterregulation by IL-10; proinflammatory cytokines; Th1-mediated intestinal disease; IL-10 therapy

Published
2000

9. Cytokine release: A workshop proceedings on the state-of-the-science, current challenges and future directions

Author

Grimaldi, Christine, primary, Finco, Deborah, additional, Fort, Madeline M., additional, Gliddon, Daniel, additional, Harper, Kirsty, additional, Helms, Whitney S., additional, Mitchell, Jane A., additional, O’Lone, Raegan, additional, Parish, Stanley T., additional, Piche, Marie-Soleil, additional, Reed, Daniel M., additional, Reichmann, Gabriele, additional, Ryan, Patricia C., additional, Stebbings, Richard, additional, and Walker, Mindi, additional

Published
2016
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12. A Synthetic TLR4 Antagonist Has Anti-Inflammatory Effects in Two Murine Models of Inflammatory Bowel Disease

Author

Fort, Madeline M., primary, Mozaffarian, Afsaneh, additional, Stöver, Axel G., additional, Correia, Jean da Silva, additional, Johnson, David A., additional, Crane, R. Thomas, additional, Ulevitch, Richard J., additional, Persing, David H., additional, Bielefeldt-Ohmann, Helle, additional, Probst, Peter, additional, Jeffery, Eric, additional, Fling, Steven P., additional, and Hershberg, Robert M., additional

Published
2005
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13. IL-25 Induces IL-4, IL-5, and IL-13 and Th2-Associated Pathologies In Vivo

Author

Fort, Madeline M., primary, Cheung, Jeanne, additional, Yen, David, additional, Li, Joana, additional, Zurawski, Sandra M., additional, Lo, Sylvia, additional, Menon, Satish, additional, Clifford, Teresa, additional, Hunte, Brisdell, additional, Lesley, Robin, additional, Muchamuel, Tony, additional, Hurst, Stephen D., additional, Zurawski, Gerard, additional, Leach, Michael W., additional, Gorman, Daniel M., additional, and Rennick, Donna M., additional

Published
2001
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22. A comparison of three nucleoside analogs with anti-retroviral activity on immune and hematopoietic functions in mice: In vitro toxicity to precursor cells and microstromal environment

Author

Luster, Michael I., primary, Germolec, Dori R., additional, White, Kimber L., additional, Fuchs, Bruce A., additional, Fort, Madeline M., additional, Tomaszewski, Joseph E., additional, Thompson, Morrow, additional, Blair, Patricia C., additional, McCay, J.Ann, additional, Munson, Albert E., additional, and Rosenthal, Gary J., additional

Published
1989
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