Search

Your search keyword '"Ruff, William E."' showing total 10 results
Start Over Author "Ruff, William E." Publication Year Range Last 3 years
10 results on '"Ruff, William E."'

1. Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis

Author

Asashima, Hiromitsu, Axisa, Pierre-Paul, Pham, Thi Hong Giang, Longbrake, Erin E., Ruff, William E., Lele, Nikhil, Cohen, Inessa, Raddassi, Khadir, Sumida, Tomokazu S., and Hafler, David A.

Subjects
Physiological aspects, Development and progression, Health aspects, B cells -- Physiological aspects -- Health aspects, Multiple sclerosis -- Development and progression, CD4 lymphocytes -- Physiological aspects -- Health aspects
Abstract

Introduction Relapsing-remitting multiple sclerosis (RRMS) is a genetically mediated autoimmune disease mediated by mye[Lin.sup.-]reactive T cells attacking the CNS (1-3) and is characterized by inflammatory lesions predominantly in the white [...], B cell depletion in patients with relapsing-remitting multiple sclerosis (RRMS) markedly prevents new MRI-detected lesions and disease activity, suggesting the hypothesis that altered B cell function leads to the activation of T cells driving disease pathogenesis. Here, we performed comprehensive analyses of CD40 ligand- (CD40L-) and IL-21-stimulated memory B cells from patients with MS and healthy age-matched controls, modeling the help of follicular helper T cells (Tfh cells), and found a differential gene expression signature in multiple B cell pathways. Most striking was the impaired TIGIT expression on MS-derived B cells mediated by dysregulation of the transcription factor TCF4. Activated circulating Tfh cells (cTfh cells) expressed CD155, the ligand of TIGIT, and TIGIT on B cells revealed their capacity to suppress the proliferation of IL-17- producing cTfh cells via the TIGIT/CD155 axis. Finally, [CCR6.sup.+] cTfh cells were significantly increased in patients with MS, and their frequency was inversely correlated with that of [TIGIT.sup.+] B cells. Together, these data suggest that the dysregulation of negative feedback loops between [TIGIT.sup.+] memory B cells and cTfh cells in MS drives the activated immune system in this disease.

Published
2022
Full Text
View/download PDF

2. Phenotypes of disease severity in a cohort of hospitalized COVID-19 patients: Results from the IMPACC study

Author

Ozonoff, Al, Schaenman, Joanna, Jayavelu, Naresh Doni, Milliren, Carly E., Calfee, Carolyn S., Cairns, Charles B., Kraft, Monica, Baden, Lindsey R., Shaw, Albert C., Krammer, Florian, van Bakel, Harm, Esserman, Denise A., Liu, Shanshan, Sesma, Ana Fernandez, Simon, Viviana, Hafler, David A., Montgomery, Ruth R., Kleinstein, Steven H., Levy, Ofer, Bime, Chris, Haddad, Elias K., Erle, David J., Pulendran, Bali, Nadeau, Kari C., Davis, Mark M, Hough, Catherine L., Messer, William B., Higuita, Nelson I. Agudelo, Metcalf, Jordan P., Atkinson, Mark A., Brakenridge, Scott C., Corry, David, Kheradmand, Farrah, Ehrlich, Lauren I.R., Melamed, Esther, McComsey, Grace A., Sekaly, Rafick, Diray-Arce, Joann, Peters, Bjoern, Augustine, Alison D., Reed, Elaine F., McEnaney, Kerry, Barton, Brenda, Lentucci, Claudia, Saluvan, Mehmet, Chang, Ana C., Hoch, Annmarie, Albert, Marisa, Shaheen, Tanzia, Kho, Alvin T., Thomas, Sanya, Chen, Jing, Murphy, Maimouna D., Cooney, Mitchell, Presnell, Scott, Fragiadakis, Gabriela K., Patel, Ravi, Guan, Leying, Gygi, Jeremy, Pawar, Shrikant, Brito, Anderson, Khalil, Zain, Maguire, Cole, Fourati, Slim, Overton, James A., Vita, Randi, Westendorf, Kerstin, Salehi-Rad, Ramin, Leligdowicz, Aleksandra, Matthay, Michael A., Singer, Jonathan P., Kangelaris, Kirsten N., Hendrickson, Carolyn M., Krummel, Matthew F., Langelier, Charles R., Woodruff, Prescott G., Powell, Debra L., Kim, James N., Simmons, Brent, Goonewardene, I. Michael, Smith, Cecilia M., Martens, Mark, Mosier, Jarrod, Kimura, Hiroki, Sherman, Amy C., Walsh, Stephen R., Issa, Nicolas C., Dela Cruz, Charles, Farhadian, Shelli, Iwasaki, Akiko, Ko, Albert I., Chinthrajah, Sharon, Ahuja, Neera, Rogers, Angela J., Artandi, Maja, Siegel, Sarah A.R., Lu, Zhengchun, Drevets, Douglas A., Brown, Brent R., Anderson, Matthew L., Guirgis, Faheem W., Thyagarajan, Rama V., Rousseau, Justin F., Wylie, Dennis, Busch, Johanna, Gandhi, Saurin, Triplett, Todd A., Yendewa, George, Giddings, Olivia, Anderson, Evan J., Mehta, Aneesh K., Sevransky, Jonathan E., Khor, Bernard, Rahman, Adeeb, Stadlbauer, Daniel, Dutta, Jayeeta, Xie, Hui, Kim-Schulze, Seunghee, Gonzalez-Reiche, Ana Silvia, van de Guchte, Adriana, Farrugia, Keith, Khan, Zenab, Maecker, Holden T., Elashoff, David, Brook, Jenny, Ramires-Sanchez, Estefania, Llamas, Megan, Rivera, Adreanne, Perdomo, Claudia, Ward, Dawn C., Magyar, Clara E., Fulcher, Jennifer A., Abe-Jones, Yumiko, Asthana, Saurabh, Beagle, Alexander, Bhide, Sharvari, Carrillo, Sidney A., Chak, Suzanna, Ghale, Rajani, Gonzalez, Ana, Jauregui, Alejandra, Jones, Norman, Lea, Tasha, Lee, Deanna, Lota, Raphael, Milush, Jeff, Nguyen, Viet, Pierce, Logan, Prasad, Priya A., Rao, Arjun, Samad, Bushra, Shaw, Cole, Sigman, Austin, Sinha, Pratik, Ward, Alyssa, Willmore, Andrew, Zhan, Jenny, Rashid, Sadeed, Rodriguez, Nicklaus, Tang, Kevin, Altamirano, Luz Torres, Betancourt, Legna, Curiel, Cindy, Sutter, Nicole, Paz, Maria Tercero, Tietje-Ulrich, Gayelan, Leroux, Carolyn, Connors, Jennifer, Bernui, Mariana, Kutzler, Michel A., Edwards, Carolyn, Lee, Edward, Lin, Edward, Croen, Brett, Semenza, Nicholas C., Rogowski, Brandon, Melnyk, Nataliya, Woloszczuk, Kyra, Cusimano, Gina, Bell, Mathew R., Furukawa, Sara, McLin, Renee, Marrero, Pamela, Sheidy, Julie, Tegos, George P., Nagle, Crystal, Mege, Nathan, Ulring, Kristen, Seyfert-Margolis, Vicki, Conway, Michelle, Francisco, Dave, Molzahn, Allyson, Erickson, Heidi, Wilson, Connie Cathleen, Schunk, Ron, Sierra, Bianca, Hughes, Trina, Smolen, Kinga, Desjardins, Michael, van Haren, Simon, Mitre, Xhoi, Cauley, Jessica, Li, Xiaofang, Tong, Alexandra, Evans, Bethany, Montesano, Christina, Licona, Jose Humberto, Krauss, Jonathan, Chang, Jun Bai Park, Izaguirre, Natalie, Chaudhary, Omkar, Coppi, Andreas, Fournier, John, Mohanty, Subhasis, Muenker, M. Catherine, Nelson, Allison, Raddassi, Khadir, Rainone, Michael, Ruff, William E., Salahuddin, Syim, Schulz, Wade L., Vijayakumar, Pavithra, Wang, Haowei, Wunder Jr., Elsio, Young, H. Patrick, Zhao, Yujiao, Saksena, Miti, Altman, Deena, Kojic, Erna, Srivastava, Komal, Eaker, Lily Q., Bermúdez-González, Maria C., Beach, Katherine F., Sominsky, Levy A., Azad, Arman R., Carreño, Juan Manuel, Singh, Gagandeep, Raskin, Ariel, Tcheou, Johnstone, Bielak, Dominika, Kawabata, Hisaaki, Mulder, Lubbertus CF, Kleiner, Giulio, Lee, Alexandra S., Do, Evan Do, Fernandes, Andrea, Manohar, Monali, Hagan, Thomas, Blish, Catherine A., Din, Hena Naz, Roque, Jonasel, Yang, Samuel, Brunton, Amanda, Sullivan, Peter E., Strnad, Matthew, Lyski, Zoe L., Coulter, Felicity J., Booth, J. Leland, Sinko, Lauren A., Moldawer, Lyle L., Borresen, Brittany, Roth-Manning, Brittney, Song, Li-Zhen, Nelson, Ebony, Lewis-Smith, Megan, Smith, Jacob, Tipan, Pablo Guaman, Siles, Nadia, Bazzi, Sam, Geltman, Janelle, Hurley, Kerin, Gabriele, Gio, Sieg, Scott, Vaysman, Tatyana, Bristow, Laurel, Hussaini, Laila, Hellmeister, Kieffer, Samaha, Hady, Cheng, Andrew, Spainhour, Christine, Scherer, Erin M., Johnson, Brandi, Bechnak, Amer, Ciric, Caroline R., Hewitt, Lauren, Carter, Erin, Mcnair, Nina, Panganiban, Bernadine, Huerta, Christopher, Usher, Jacob, Ribeiro, Susan Pereira, Altman, Matthew C., Becker, Patrice M., Rouphael, Nadine, Bime, Christian, and Davis, Mark M.

Published
2022
Full Text
View/download PDF

3. The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository in the AIRR Data Commons: a practical guide for access, use and contributions through the Type 1 Diabetes AIRR Consortium.

Author

Hanna, Stephanie J., Bonami, Rachel H., Corrie, Brian, Westley, Monica, Posgai, Amanda L., Luning Prak, Eline T., Breden, Felix, Michels, Aaron W., Brusko, Todd M., Baschal, Erin, Cerosaletti, Karen, Corrie, Lorissa, Gomez-Tourino, Iria, Higdon, Lauren, Kent, Sally C., Linsley, Peter, Nakayama, Maki, Neller, Kira, Ruff, William E., and Teyton, Luc

Abstract

Human molecular genetics has brought incredible insights into the variants that confer risk for the development of tissue-specific autoimmune diseases, including type 1 diabetes. The hallmark cell-mediated immune destruction that is characteristic of type 1 diabetes is closely linked with risk conferred by the HLA class II gene locus, in combination with a broad array of additional candidate genes influencing islet-resident beta cells within the pancreas, as well as function, phenotype and trafficking of immune cells to tissues. In addition to the well-studied germline SNP variants, there are critical contributions conferred by T cell receptor (TCR) and B cell receptor (BCR) genes that undergo somatic recombination to yield the Adaptive Immune Receptor Repertoire (AIRR) responsible for autoimmunity in type 1 diabetes. We therefore created the T1D TCR/BCR Repository (The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository) to study these highly variable and dynamic gene rearrangements. In addition to processed TCR and BCR sequences, the T1D TCR/BCR Repository includes detailed metadata (e.g. participant demographics, disease-associated parameters and tissue type). We introduce the Type 1 Diabetes AIRR Consortium goals and outline methods to use and deposit data to this comprehensive repository. Our ultimate goal is to facilitate research community access to rich, carefully annotated immune AIRR datasets to enable new scientific inquiry and insight into the natural history and pathogenesis of type 1 diabetes. [ABSTRACT FROM AUTHOR]

Published
2025
Full Text
View/download PDF

5. Single-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19

Author

Unterman, Avraham, Sumida, Tomokazu S., Nouri, Nima, Yan, Xiting, Zhao, Amy Y., Gasque, Victor, Schupp, Jonas C., Asashima, Hiromitsu, Liu, Yunqing, Cosme, Jr., Carlos, Deng, Wenxuan, Chen, Ming, Raredon, Micha Sam Brickman, Hoehn, Kenneth B., Wang, Guilin, Wang, Zuoheng, DeIuliis, Giuseppe, Ravindra, Neal G., Li, Ningshan, Castaldi, Christopher, Wong, Patrick, Fournier, John, Bermejo, Santos, Sharma, Lokesh, Casanovas-Massana, Arnau, Vogels, Chantal B. F., Wyllie, Anne L., Grubaugh, Nathan D., Melillo, Anthony, Meng, Hailong, Stein, Yan, Minasyan, Maksym, Mohanty, Subhasis, Ruff, William E., Cohen, Inessa, Raddassi, Khadir, Niklason, Laura E., Ko, Albert I., Montgomery, Ruth R., Farhadian, Shelli F., Iwasaki, Akiko, Shaw, Albert C., van Dijk, David, Zhao, Hongyu, Kleinstein, Steven H., Hafler, David A., Kaminski, Naftali, and Dela Cruz, Charles S.

Published
2022
Full Text
View/download PDF

6. Prior cycles of anti-CD20 antibodies affect antibody responses after repeated SARS-CoV-2 mRNA vaccination

Author

Asashima, Hiromitsu, primary, Kim, Dongjoo, additional, Wang, Kaicheng, additional, Lele, Nikhil, additional, Buitrago-Pocasangre, Nicholas C., additional, Lutz, Rachel, additional, Cruz, Isabella, additional, Raddassi, Khadir, additional, Ruff, William E., additional, Racke, Michael K., additional, Wilson, JoDell E., additional, Givens, Tara S., additional, Grifoni, Alba, additional, Weiskopf, Daniela, additional, Sette, Alessandro, additional, Kleinstein, Steven H., additional, Montgomery, Ruth R., additional, Shaw, Albert C., additional, Li, Fangyong, additional, Fan, Rong, additional, Hafler, David A., additional, Tomayko, Mary M., additional, and Longbrake, Erin E., additional

Published
2023
Full Text
View/download PDF

7. PD-1highCXCR5–CD4+ peripheral helper T cells promote CXCR3+ plasmablasts in human acute viral infection

Author

Asashima, Hiromitsu, primary, Mohanty, Subhasis, additional, Comi, Michela, additional, Ruff, William E., additional, Hoehn, Kenneth B., additional, Wong, Patrick, additional, Klein, Jon, additional, Lucas, Carolina, additional, Cohen, Inessa, additional, Coffey, Sarah, additional, Lele, Nikhil, additional, Greta, Leissa, additional, Raddassi, Khadir, additional, Chaudhary, Omkar, additional, Unterman, Avraham, additional, Emu, Brinda, additional, Kleinstein, Steven H., additional, Montgomery, Ruth R., additional, Iwasaki, Akiko, additional, Dela Cruz, Charles S., additional, Kaminski, Naftali, additional, Shaw, Albert C., additional, Hafler, David A., additional, and Sumida, Tomokazu S., additional

Published
2023
Full Text
View/download PDF

8. PD-1highCXCR5–CD4+peripheral helper T cells promote CXCR3+plasmablasts in human acute viral infection

Author

Asashima, Hiromitsu, Mohanty, Subhasis, Comi, Michela, Ruff, William E., Hoehn, Kenneth B., Wong, Patrick, Klein, Jon, Lucas, Carolina, Cohen, Inessa, Coffey, Sarah, Lele, Nikhil, Greta, Leissa, Raddassi, Khadir, Chaudhary, Omkar, Unterman, Avraham, Emu, Brinda, Kleinstein, Steven H., Montgomery, Ruth R., Iwasaki, Akiko, Dela Cruz, Charles S., Kaminski, Naftali, Shaw, Albert C., Hafler, David A., and Sumida, Tomokazu S.

Abstract

T cell-B cell interaction is the key immune response to protect the host from severe viral infection. However, how T cells support B cells to exert protective humoral immunity in humans is not well understood. Here, we use COVID-19 as a model of acute viral infections and analyze CD4+T cell subsets associated with plasmablast expansion and clinical outcome. Peripheral helper T cells (Tph cells; denoted as PD-1highCXCR5–CD4+T cells) are significantly increased, as are plasmablasts. Tph cells exhibit “B cell help” signatures and induce plasmablast differentiation in vitro. Interestingly, expanded plasmablasts show increased CXCR3expression, which is positively correlated with higher frequency of activated Tph cells and better clinical outcome. Mechanistically, Tph cells help B cell differentiation and produce more interferon γ (IFNγ), which induces CXCR3 expression on plasmablasts. These results elucidate a role for Tph cells in regulating protective B cell response during acute viral infection.

Published
2023
Full Text
View/download PDF

9. Malignant T Cell Activation by a BacillusSpecies Isolated from Cutaneous T-Cell Lymphoma Lesions

Author

Dehner, Carina A., Ruff, William E., Greiling, Teri, Pereira, Márcia S., Redanz, Sylvio, McNiff, Jennifer, Girardi, Michael, and Kriegel, Martin A.

Abstract

Cutaneous T-cell lymphoma (CTCL) is a life-debilitating malignancy of lymphocytes homing to the skin. Although CTCL is thought to arise from a combination of genetic, epigenetic, and environmental factors, specific triggers are unclear. The skin is colonized by a unique microbiota and is heavily influenced by its interactions. We hypothesized that adaptive immune responses to skin commensals lead to clonal T-cell proliferation and transformation in the appropriate genetic background. We therefore collected lesional and nonlesional skin microbiota from patients with CTCL to study T cell interactions using skin T cell explants and peripheral, skin-homing CD4+T cells. By various methods, we identified Bacillus safensisin CTCL lesions, a rare human commensal in healthy skin, and showed that it can induce malignant T cell activation and cytokine secretion. Taken together, our data suggest microbial triggers in the skin microbiota of patients with CTCL as potential instigators of tumorigenesis.

Published
2022
Full Text
View/download PDF

10. Alterations in Gut Microbiome-Host Relationships After Immune Perturbation in Patients With Multiple Sclerosis.

Author

Gupta VK, Janda GS, Pump HK, Lele N, Cruz I, Cohen I, Ruff WE, Hafler DA, Sung J, and Longbrake EE

Subjects
Humans, Male, Female, Adult, Middle Aged, RNA, Ribosomal, 16S, Gastrointestinal Microbiome immunology, Multiple Sclerosis immunology, Multiple Sclerosis microbiology, Immunoglobulin A immunology
Abstract

Background and Objectives: Gut microbial symbionts have been shown to influence the development of autoimmunity in multiple sclerosis (MS). Emerging research points to an important relationship between the microbial-IgA interface and MS pathophysiology. IgA-secreting B cells are observed in the MS brain, and shifts in gut bacteria-IgA binding have been described in some patients with MS. However, the relationships between the gut microbiome and the host immune response, particularly regarding B-cell-depleting immunomodulation, remain underexplored. This study aimed to evaluate the composition of the gut microbiome in patients with newly diagnosed MS at baseline and after B-cell depletion, using long-read sequencing for enhanced taxonomic resolution. We further aimed to investigate the host/microbiome interface by evaluating microbe/immunoglobulin A relationships., Methods: We collected stool samples from 43 patients with newly diagnosed, untreated MS and 42 matched healthy controls. Nineteen patients with MS initiated anti-CD20 monoclonal antibody treatment and donated additional stool samples after 6 months of treatment. We evaluated the host-microbial interface using bacterial flow cytometry and long-read 16S rRNA gene amplicon sequencing. We used Immune Coating Scores to compare the proportions of bacteria identified in the IgA-coated vs IgA-uncoated bacterial fractions., Results: Patients with untreated, newly diagnosed MS showed significant reductions in IgA-bound fecal microbiota compared with controls. Using multiple linear regression models adjusted for potential confounders, we observed significant ( p < 0.05) changes in the abundance and prevalence of various strain-level gut bacteria amplicon sequence variants (ASVs) within both total and IgA-coated bacterial fractions. Some changes (e.g., decreased relative abundance of a Faecalibacterium prausnitzii variant in MS) were consistent with previous reports, while others (e.g., increased relative abundance and prevalence of Monoglobus pectinyliticus in MS) were novel. Immune Coating Scores identified subsets of organisms for which normal IgA-coating patterns were disrupted at the onset of MS, as well as those (particularly Akkermansia muciniphila ) whose IgA-coating became more aligned with controls after therapy., Discussion: This analysis of gut microbial ASVs reveals shifts in taxonomic strains induced by immune modulation in MS.

Published
2025
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results