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7 results on '"Barber, Daniel L."'

1. Response to Comments on “Aberrant type 1 immunity drives susceptibility to mucosal fungal infections”

Author

Break, Timothy J, Oikonomou, Vasileios, Dutzan, Nicolas, Desai, Jigar V, Swidergall, Marc, Freiwald, Tilo, Chauss, Daniel, Harrison, Oliver J, Alejo, Julie, Williams, Drake W, Pittaluga, Stefania, Lee, Chyi-Chia R, Bouladoux, Nicolas, Swamydas, Muthulekha, Hoffman, Kevin W, Greenwell-Wild, Teresa, Bruno, Vincent M, Rosen, Lindsey B, Lwin, Wint, Renteria, Andy, Pontejo, Sergio M, Shannon, John P, Myles, Ian A, Olbrich, Peter, Ferré, Elise MN, Schmitt, Monica, Martin, Daniel, Core16, Genomics and Computational Biology, Barber, Daniel L, Solis, Norma V, Notarangelo, Luigi D, Serreze, David V, Matsumoto, Mitsuru, Hickman, Heather D, Murphy, Philip M, Anderson, Mark S, Lim, Jean K, Holland, Steven M, Filler, Scott G, Afzali, Behdad, Belkaid, Yasmine, Moutsopoulos, Niki M, and Lionakis, Michail S

Subjects
Autoimmune Disease, Clinical Research, Infectious Diseases, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Humans, Immunity, Mucosal, Mucous Membrane, Mycoses, Genomics and Computational Biology Core16, General Science & Technology
Abstract

Puel and Casanova and Kisand et al. challenge our conclusions that interferonopathy and not IL-17/IL-22 autoantibodies promote candidiasis in autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy. We acknowledge that conclusive evidence for causation is difficult to obtain in complex human diseases. However, our studies clearly document interferonopathy driving mucosal candidiasis with intact IL-17/IL-22 responses in Aire-deficient mice, with strong corroborative evidence in patients.

Published
2021

2. Aberrant type 1 immunity drives susceptibility to mucosal fungal infections

Author

Break, Timothy J, Oikonomou, Vasileios, Dutzan, Nicolas, Desai, Jigar V, Swidergall, Marc, Freiwald, Tilo, Chauss, Daniel, Harrison, Oliver J, Alejo, Julie, Williams, Drake W, Pittaluga, Stefania, Lee, Chyi-Chia R, Bouladoux, Nicolas, Swamydas, Muthulekha, Hoffman, Kevin W, Greenwell-Wild, Teresa, Bruno, Vincent M, Rosen, Lindsey B, Lwin, Wint, Renteria, Andy, Pontejo, Sergio M, Shannon, John P, Myles, Ian A, Olbrich, Peter, Ferré, Elise MN, Schmitt, Monica, Martin, Daniel, Core16, Genomics and Computational Biology, Barber, Daniel L, Solis, Norma V, Notarangelo, Luigi D, Serreze, David V, Matsumoto, Mitsuru, Hickman, Heather D, Murphy, Philip M, Anderson, Mark S, Lim, Jean K, Holland, Steven M, Filler, Scott G, Afzali, Behdad, Belkaid, Yasmine, Moutsopoulos, Niki M, and Lionakis, Michail S

Subjects
Autoimmune Disease, Emerging Infectious Diseases, Infectious Diseases, 2.1 Biological and endogenous factors, Aetiology, Infection, Inflammatory and immune system, Adolescent, Adult, Aged, Animals, Candida albicans, Candidiasis, Chronic Mucocutaneous, Disease Models, Animal, Female, Humans, Immunity, Mucosal, Immunologic Surveillance, Interferon-gamma, Interleukins, Janus Kinases, Male, Mice, Mice, Inbred BALB C, Middle Aged, Mouth Mucosa, Polyendocrinopathies, Autoimmune, Receptors, Interleukin-17, STAT1 Transcription Factor, T-Lymphocytes, Young Adult, Genomics and Computational Biology Core, General Science & Technology
Abstract

Human monogenic disorders have revealed the critical contribution of type 17 responses in mucosal fungal surveillance. We unexpectedly found that in certain settings, enhanced type 1 immunity rather than defective type 17 responses can promote mucosal fungal infection susceptibility. Notably, in mice and humans with AIRE deficiency, an autoimmune disease characterized by selective susceptibility to mucosal but not systemic fungal infection, mucosal type 17 responses are intact while type 1 responses are exacerbated. These responses promote aberrant interferon-γ (IFN-γ)- and signal transducer and activator of transcription 1 (STAT1)-dependent epithelial barrier defects as well as mucosal fungal infection susceptibility. Concordantly, genetic and pharmacologic inhibition of IFN-γ or Janus kinase (JAK)-STAT signaling ameliorates mucosal fungal disease. Thus, we identify aberrant T cell-dependent, type 1 mucosal inflammation as a critical tissue-specific pathogenic mechanism that promotes mucosal fungal infection susceptibility in mice and humans.

Published
2021

3. Rescue of exhausted CD8 T cells by PD-1–targeted therapies is CD28-dependent

Author

Kamphorst, Alice O., Wieland, Andreas, Nasti, Tahseen, Yang, Shu, Zhang, Ruan, Barber, Daniel L., Konieczny, Bogumila T., Daugherty, Candace Z., Koenig, Lydia, Yu, Ke, Sica, Gabriel L., Sharpe, Arlene H., Freeman, Gordon J., Blazar, Bruce R., Turka, Laurence A., Owonikoko, Taofeek K., Pillai, Rathi N., Ramalingam, Suresh S., Araki, Koichi, and Ahmed, Rafi

Published
2017

4. Vaccine-elicited CD4 T cells induce immunopathology after chronic LCMV infection

Author

Penaloza-MacMaster, Pablo, Barber, Daniel L., Wherry, E. John, Provine, Nicholas M., Teigler, Jeffrey E., Parenteau, Lily, Blackmore, Stephen, Borducchi, Erica N., Larocca, Rafael A., Yates, Kathleen B., Shen, Hao, Haining, W. Nicholas, Sommerstein, Rami, Pinschewer, Daniel D., Ahmed, Rafi, and Barouch, Dan H.

Published
2015

7. Visualizing Antigen-Specific and Infected Cells in Situ Predicts Outcomes in Early Viral Infection.

Author

Qingsheng Li, Skinner, Pamela J., Sang-Jun Ha, Duan, Lijie, Mattila, Teresa L., Hage, Aaron, White, Cara, Barber, Daniel L., O'Mara, Leigh, Southern, Peter J., Reilly, Cavan S., Carlis, John V., Miller, Christopher J., Ahmed, Rafi, and Haase, Ashley T.

Subjects
*ANTIGENS, *VIRUS diseases, *IMMUNE response, *CELLS, *HIV infections, *SIMIAN viruses, *LYMPHOCYTIC choriomeningitis virus
Abstract

In the early stages of viral infection, outcomes depend on a race between expansion of infection and the immune response generated to contain it. We combined in situ tetramer staining with in situ hybridization to visualize, map, and quantify relationships between immune effector cells and their targets in tissues. In simian immunodeficiency virus infections in macaques and lymphocytic choriomeningitis virus infections in mice, the magnitude and timing of the establishment of ah excess of effector cells versus targets were found to correlate with the extent of control and the infection outcome (i.e., control and clearance versus partial or poor control and persistent infection). This method highlights the importance of the location, timing, and magnitude of the immune response needed for a vaccine to be effective against agents of persistent infection, such as HIV-1. [ABSTRACT FROM AUTHOR]

Published
2009

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