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Your search keyword '"Abdel-Mohsen, Mohamed"' showing total 6 results
Start Over Author "Abdel-Mohsen, Mohamed" Journal nature communications
6 results on '"Abdel-Mohsen, Mohamed"'

1. Non-human primate model of long-COVID identifies immune associates of hyperglycemia

Author

Palmer, Clovis S., Perdios, Chrysostomos, Abdel-Mohsen, Mohamed, Mudd, Joseph, Datta, Prasun K., Maness, Nicholas J., Lehmicke, Gabrielle, Golden, Nadia, Hellmers, Linh, Coyne, Carol, Moore Green, Kristyn, Midkiff, Cecily, Williams, Kelsey, Tiburcio, Rafael, Fahlberg, Marissa, Boykin, Kyndal, Kenway, Carys, Russell-Lodrigue, Kasi, Birnbaum, Angela, Bohm, Rudolf, Blair, Robert, Dufour, Jason P., Fischer, Tracy, Saied, Ahmad A., and Rappaport, Jay

Published
2024
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2. Immunoglobulin G N-glycan markers of accelerated biological aging during chronic HIV infection

Author

Giron, Leila B., Liu, Qin, Adeniji, Opeyemi S., Yin, Xiangfan, Kannan, Toshitha, Ding, Jianyi, Lu, David Y., Langan, Susan, Zhang, Jinbing, Azevedo, Joao L. L. C., Li, Shuk Hang, Shalygin, Sergei, Azadi, Parastoo, Hanna, David B., Ofotokun, Igho, Lazar, Jason, Fischl, Margaret A., Haberlen, Sabina, Macatangay, Bernard, Adimora, Adaora A., Jamieson, Beth D., Rinaldo, Charles, Merenstein, Daniel, Roan, Nadia R., Kutsch, Olaf, Gange, Stephen, Wolinsky, Steven M., Witt, Mallory D., Post, Wendy S., Kossenkov, Andrew, Landay, Alan L., Frank, Ian, Tien, Phyllis C., Gross, Robert, Brown, Todd T., and Abdel-Mohsen, Mohamed

Published
2024
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4. Estimating the contribution of CD4 T cell subset proliferation and differentiation to HIV persistence

Author

Reeves, Daniel B, Bacchus-Souffan, Charline, Fitch, Mark, Abdel-Mohsen, Mohamed, Hoh, Rebecca, Ahn, Haelee, Stone, Mars, Hecht, Frederick, Martin, Jeffrey, Deeks, Steven G, Hellerstein, Marc K, McCune, Joseph M, Schiffer, Joshua T, and Hunt, Peter W

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Clinical Research, HIV/AIDS, Sexually Transmitted Infections, Infectious Diseases, Humans, Male, CD4-Positive T-Lymphocytes, DNA, Viral, HIV-1, T-Lymphocyte Subsets, HIV Infections, Cell Proliferation, Cell Differentiation, Hyperplasia, Immunologic Memory
Abstract

Persistence of HIV in people living with HIV (PWH) on suppressive antiretroviral therapy (ART) has been linked to physiological mechanisms of CD4+ T cells. Here, in the same 37 male PWH on ART we measure longitudinal kinetics of HIV DNA and cell turnover rates in five CD4 cell subsets: naïve (TN), stem-cell- (TSCM), central- (TCM), transitional- (TTM), and effector-memory (TEM). HIV decreases in TTM and TEM but not in less-differentiated subsets. Cell turnover is ~10 times faster than HIV clearance in memory subsets, implying that cellular proliferation consistently creates HIV DNA. The optimal mathematical model for these integrated data sets posits HIV DNA also passages between CD4 cell subsets via cellular differentiation. Estimates are heterogeneous, but in an average participant's year ~10 (in TN and TSCM) and ~104 (in TCM, TTM, TEM) proviruses are generated by proliferation while ~103 proviruses passage via cell differentiation (per million CD4). In simulations, therapies blocking proliferation and/or enhancing differentiation could reduce HIV DNA by 1-2 logs over 3 years. In summary, HIV exploits cellular proliferation and differentiation to persist during ART but clears faster in more proliferative/differentiated CD4 cell subsets and the same physiological mechanisms sustaining HIV might be temporarily modified to reduce it.

Published
2023

5. Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy.

Author

Somasundaram, Rajasekharan, Connelly, Thomas, Choi, Robin, Choi, Hyeree, Samarkina, Anastasia, Li, Ling, Gregorio, Elizabeth, Chen, Yeqing, Thakur, Rohit, Abdel-Mohsen, Mohamed, Beqiri, Marilda, Kiernan, Meaghan, Perego, Michela, Wang, Fang, Xiao, Min, Brafford, Patricia, Yang, Xue, Xu, Xiaowei, Secreto, Anthony, Danet-Desnoyers, Gwenn, Traum, Daniel, Kaestner, Klaus H, Huang, Alexander C, Hristova, Denitsa, Wang, Joshua, Fukunaga-Kalabis, Mizuho, Krepler, Clemens, Ping-Chen, Fang, Zhou, Xiangyang, Gutierrez, Alexis, Rebecca, Vito W, Vonteddu, Prashanthi, Dotiwala, Farokh, Bala, Shashi, Majumdar, Sonali, Dweep, Harsh, Wickramasinghe, Jayamanna, Kossenkov, Andrew V, Reyes-Arbujas, Jorge, Santiago, Kenisha, Nguyen, Tran, Griss, Johannes, Keeney, Frederick, Hayden, James, Gavin, Brian J, Weiner, David, Montaner, Luis J, Liu, Qin, Peiffer, Lukas, Becker, Jürgen, Burton, Elizabeth M, Davies, Michael A, Tetzlaff, Michael T, Muthumani, Kar, Wargo, Jennifer A, Gabrilovich, Dmitry, and Herlyn, Meenhard

Subjects
B-Lymphocytes, T-Lymphocytes, Lymphocytes, Tumor-Infiltrating, Mast Cells, Animals, Mice, Transgenic, Humans, Melanoma, Drug Resistance, Neoplasm, Programmed Cell Death 1 Receptor, Sunitinib, Immune Checkpoint Inhibitors
Abstract

Anti-PD-1 therapy is used as a front-line treatment for many cancers, but mechanistic insight into this therapy resistance is still lacking. Here we generate a humanized (Hu)-mouse melanoma model by injecting fetal liver-derived CD34+ cells and implanting autologous thymus in immune-deficient NOD-scid IL2Rγnull (NSG) mice. Reconstituted Hu-mice are challenged with HLA-matched melanomas and treated with anti-PD-1, which results in restricted tumor growth but not complete regression. Tumor RNA-seq, multiplexed imaging and immunohistology staining show high expression of chemokines, as well as recruitment of FOXP3+ Treg and mast cells, in selective tumor regions. Reduced HLA-class I expression and CD8+/Granz B+ T cells homeostasis are observed in tumor regions where FOXP3+ Treg and mast cells co-localize, with such features associated with resistance to anti-PD-1 treatment. Combining anti-PD-1 with sunitinib or imatinib results in the depletion of mast cells and complete regression of tumors. Our results thus implicate mast cell depletion for improving the efficacy of anti-PD-1 therapy.

Published
2021

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