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25 results on '"Moffett, Howell F."'

8. Erratum: The microRNA miR-31 inhibits CD8+ T cell function in chronic viral infection

Author

Moffett, Howell F, primary, Cartwright, Adam N R, additional, Kim, Hye-Jung, additional, Godec, Jernej, additional, Pyrdol, Jason, additional, Äijö, Tarmo, additional, Martinez, Gustavo J, additional, Rao, Anjana, additional, Lu, Jun, additional, Golub, Todd R, additional, Cantor, Harvey, additional, Sharpe, Arlene H, additional, Novina, Carl D, additional, and Wucherpfennig, Kai W, additional

Published
2017
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9. The microRNA miR-31 inhibits CD8+ T cell function in chronic viral infection

Author

Moffett, Howell F, primary, Cartwright, Adam N R, additional, Kim, Hye-Jung, additional, Godec, Jernej, additional, Pyrdol, Jason, additional, Äijö, Tarmo, additional, Martinez, Gustavo J, additional, Rao, Anjana, additional, Lu, Jun, additional, Golub, Todd R, additional, Cantor, Harvey, additional, Sharpe, Arlene H, additional, Novina, Carl D, additional, and Wucherpfennig, Kai W, additional

Published
2017
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12. The microRNA miR-31 inhibits CD8+T cell function in chronic viral infection

Author

Moffett, Howell F, Cartwright, Adam N R, Kim, Hye-Jung, Godec, Jernej, Pyrdol, Jason, Äijö, Tarmo, Martinez, Gustavo J, Rao, Anjana, Lu, Jun, Golub, Todd R, Cantor, Harvey, Sharpe, Arlene H, Novina, Carl D, and Wucherpfennig, Kai W

Abstract

During infection, antigen-specific T cells undergo tightly regulated developmental transitions controlled by transcriptional and post-transcriptional regulation of gene expression. We found that the microRNA miR-31 was strongly induced by activation of the T cell antigen receptor (TCR) in a pathway involving calcium and activation of the transcription factor NFAT. During chronic infection with lymphocytic choriomeningitis virus (LCMV) clone 13, miR-31-deficent mice recovered from clinical disease, while wild-type mice continued to show signs of disease. This disease phenotype was explained by the presence of larger numbers of cytokine-secreting LCMV-specific CD8+T cells in miR-31-deficent mice than in wild-type mice. Mechanistically, miR-31 increased the sensitivity of T cells to type I interferons, which interfered with effector T cell function and increased the expression of several proteins related to T cell dysfunction during chronic infection. These studies identify miR-31 as an important regulator of T cell exhaustion in chronic infection.

Published
2017
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16. Heat Shock Protein-Mediated Cross-Presentation of Exogenous HIV Antigen on HLA Class I and Class II

Author

SenGupta, Devi, primary, Norris, Philip J., additional, Suscovich, Todd J., additional, Hassan-Zahraee, Mina, additional, Moffett, Howell F., additional, Trocha, Alicja, additional, Draenert, Rika, additional, Goulder, Philip J. R., additional, Binder, Robert J., additional, Levey, Daniel L., additional, Walker, Bruce D., additional, Srivastava, Pramod K., additional, and Brander, Christian, additional

Published
2004
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19. MicroRNA Expression Profiling Identifies Activated B Cell Status in Chronic Lymphocytic Leukemia Cells.

Author

Shuqiang Li, Moffett, Howell F., Jun Lu, Werner, Lillian, Hao Zhang, Ritz, Jerome, Neuberg, Donna, Wucherpfennig, Kai W., Brown, Jennifer R., and Novina, Carl D.

Subjects
*CHRONIC lymphocytic leukemia, *LEUCOCYTOSIS, *CHRONIC diseases, *LYMPHOCYTES, *PRELEUKEMIA
Abstract

Chronic lymphocytic leukemia (CLL) is thought to be a disease of resting lymphocytes. However, recent data suggest that CLL cells may more closely resemble activated B cells. Using microRNA (miRNA) expression profiling of highly-enriched CLL cells from 38 patients and 9 untransformed B cells from normal donors before acute CpG activation and 5 matched B cells after acute CpG activation, we demonstrate an activated B cell status for CLL. Gene set enrichment analysis (GSEA) identified statistically-significant similarities in miRNA expression between activated B cells and CLL cells including upregulation of miR-34a, miR-155, and miR-342-3p and downregulation of miR-103, miR-181a and miR-181b. Additionally, decreased levels of two CLL signature miRNAs miR-29c and miR-223 are associated with ZAP70+ and IgVH unmutated status and with shorter time to first therapy. These data indicate an activated B cell status for CLL cells and suggest that the direction of change of individual miRNAs may predict clinical course in CLL. [ABSTRACT FROM AUTHOR]

Published
2011
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20. Beyond Help: Direct Effector Functions of Human Immunodeficiency Virus Type 1-Specific CD4+ T Cells.

Author

Norris, Philip J., Moffett, Howell F., Yang, Otto O., Kaufmann, Daniel E., Clark, Margaret J., Addo, Marylyn M., and Rosenberg, Eric S.

Subjects
*HIV, *CD4 antigen, *T cells, *VIRAL replication, *ANTIVIRAL agents, *ANTIGENS
Abstract

The immune correlates of protection in human immunodeficiency virus type 1 (HIV-1) infection remain poorly defined, particularly the contribution of CD4+ T cells. Here we explore the effector functions of HIV-1-specific CD4 T cells. We demonstrate HIV-1 p24-specific CD4 -T-cell cytolytic activity in peripheral blood mononuclear cells directly ex vivo and after enrichment by antigen-specific stimulation. We further show that in a rare long-term nonprogressor, both an HIV-1-specific CD4+ T-cell clone and CD4+ T cells directly ex vivo exert potent suppression of HIV-1 replication. Suppression of viral replication was dependent on cell-cell contact between the effector CD4+ T cells and the target cells. While the antiviral effector activity of CD8+ T cells has been well documented, these results strongly suggest that HIV-1-specific CD4+ T cells are capable of directly contributing to antiviral immunity. [ABSTRACT FROM AUTHOR]

Published
2004
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21. Fine Specificity and Cross-Clade Reactivity of HIV Type 1 Gag-Specific CD4+ T Cells

Author

Norris, Philip J., Moffett, Howell F., Brander, Christian, Allen, Todd M., O'Sullivan, Kristin M., Cosimi, Lisa A., Kaufmann, Daniel E., Walker, Bruce D., and Rosenberg, Eric S.

Abstract

Despite growing evidence that HIV-1-specific CD4+ T helper (Th) cells may play a role in the control of viremia, discrete Th cell epitopes remain poorly defined. Furthermore, it is not known whether Th cell responses generated using vaccines based on clade B virus sequences will elicit immune responses that are effective in regions of the world where non-clade B viruses predominate. To address these issues we isolated CD4+ T cell clones from individuals with vigorous HIV-1-specific Th cell responses and identified the minimum epitopes recognized. The minimum peptide length required for induction of CD4+ T cell proliferation, IFN-γ secretion, and cytolytic activity ranged from 9 to 16 amino acids in the five epitopes studied. Crossclade recognition of the defined epitopes was examined for variant peptides from clades A, B, C, D, and AE. Over half the variant epitopes (17 of 32) exhibited impaired recognition, defined as less than 50% of the IFN-γ secretion elicited by B clade consensus sequence. There was no evidence for antagonistic activity mediated by the variant peptides, and despite strong responses there was no escape of autologous virus from Th responses in the epitopes we studied. Abrogated recognition of variant CD4+ T cell epitopes presents a potential obstacle to vaccine development.

Published
2004
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24. The microRNA miR-31 inhibits CD8 + T cell function in chronic viral infection.

Author

Moffett HF, Cartwright ANR, Kim HJ, Godec J, Pyrdol J, Äijö T, Martinez GJ, Rao A, Lu J, Golub TR, Cantor H, Sharpe AH, Novina CD, and Wucherpfennig KW

Subjects
Animals, Antibodies, Viral immunology, Arenaviridae Infections genetics, CD8-Positive T-Lymphocytes drug effects, Calcium metabolism, Chromatin Immunoprecipitation, Dendritic Cells immunology, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Gene Expression Profiling, Immunoblotting, Interferon Type I pharmacology, Lymphocytic choriomeningitis virus immunology, Mice, Mice, Knockout, MicroRNAs genetics, NFATC Transcription Factors metabolism, Real-Time Polymerase Chain Reaction, Arenaviridae Infections immunology, CD8-Positive T-Lymphocytes immunology, Cytokines immunology, MicroRNAs immunology, Receptors, Antigen, T-Cell immunology
Abstract

During infection, antigen-specific T cells undergo tightly regulated developmental transitions controlled by transcriptional and post-transcriptional regulation of gene expression. We found that the microRNA miR-31 was strongly induced by activation of the T cell antigen receptor (TCR) in a pathway involving calcium and activation of the transcription factor NFAT. During chronic infection with lymphocytic choriomeningitis virus (LCMV) clone 13, miR-31-deficent mice recovered from clinical disease, while wild-type mice continued to show signs of disease. This disease phenotype was explained by the presence of larger numbers of cytokine-secreting LCMV-specific CD8 + T cells in miR-31-deficent mice than in wild-type mice. Mechanistically, miR-31 increased the sensitivity of T cells to type I interferons, which interfered with effector T cell function and increased the expression of several proteins related to T cell dysfunction during chronic infection. These studies identify miR-31 as an important regulator of T cell exhaustion in chronic infection.

Published
2017
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25. Beyond help: direct effector functions of human immunodeficiency virus type 1-specific CD4(+) T cells.

Author

Norris PJ, Moffett HF, Yang OO, Kaufmann DE, Clark MJ, Addo MM, and Rosenberg ES

Subjects
CD4-Positive T-Lymphocytes virology, Cytotoxicity, Immunologic, HIV Core Protein p24 immunology, Humans, Leukocytes, Mononuclear immunology, Virus Replication immunology, CD4-Positive T-Lymphocytes immunology, HIV-1 immunology, T-Lymphocytes, Cytotoxic immunology, T-Lymphocytes, Regulatory immunology
Abstract

The immune correlates of protection in human immunodeficiency virus type 1 (HIV-1) infection remain poorly defined, particularly the contribution of CD4(+) T cells. Here we explore the effector functions of HIV-1-specific CD4(+) T cells. We demonstrate HIV-1 p24-specific CD4(+)-T-cell cytolytic activity in peripheral blood mononuclear cells directly ex vivo and after enrichment by antigen-specific stimulation. We further show that in a rare long-term nonprogressor, both an HIV-1-specific CD4(+)-T-cell clone and CD4(+) T cells directly ex vivo exert potent suppression of HIV-1 replication. Suppression of viral replication was dependent on cell-cell contact between the effector CD4(+) T cells and the target cells. While the antiviral effector activity of CD8(+) T cells has been well documented, these results strongly suggest that HIV-1-specific CD4(+) T cells are capable of directly contributing to antiviral immunity.

Published
2004
Full Text
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