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My current research resides in fields of transplantation immunology, host-defense, immunotherapies, genetics and vaccine design.
My colleagues and I have made several seminal discoveries. (1) My interest on B cell biology was sparked by my early work on molecular mechanisms of immunoglobulin gene recombination and mutation and led to the discovery that DNA mismatch repair drives B cell Ig gene hypermutation. This discovery inspired the approach to a mutable-antigen mouse platform to anticipate immune-driven evolution of antigens from mutable viruses. (2) We established that B cell and immunoglobulin diversity promote T cell development and the establishment of a diverse antigen receptor (TCR) repertoire. This observation led to current research directed at understanding how functions of B cells impact cellular immunity and regulation of immune responses in human health and disease. (3) We discovered that the TNRSF13B gene encoding a receptor (also abbreviated as TACI) expressed mostly by B cells is an immune-regulatory gene. TNRSF13B is among the most diverse gene in humans and vertebrates, TNRSF13B defines the type and intensity of innate and adaptive B cell responses, the interactions between B and T cells and in doing so also controls complement activation. Thus, while TNFRSF13B low-functioning alleles are beneficial in host defense blocking microbial transmission and epidemic spread, these same polymorphisms increase inflammation in part owing to decreasing control of complement activation. These findings suggested that TNFRSF13B gene diversity protects populations against unknown pathogens by assuring a wide array of immune responses that while disadvantageous in some individuals and in certain conditions, e.g. transplantation, will protect most against dissemination of microbes that evolved to explore the vulnerabilities of host defense. (4) We found that the fragment d of the third component of complement (C3d) markedly boosts and accelerates cellular immunity slowing and sometimes reverting progression of tumors. C3d does so by vitiating tumor induced immunosuppression, i.e. the processes that impair immune responses to tumors.
My colleagues and I have made several seminal discoveries. (1) My interest on B cell biology was sparked by my early work on molecular mechanisms of immunoglobulin gene recombination and mutation and led to the discovery that DNA mismatch repair drives B cell Ig gene hypermutation. This discovery inspired the approach to a mutable-antigen mouse platform to anticipate immune-driven evolution of antigens from mutable viruses. (2) We established that B cell and immunoglobulin diversity promote T cell development and the establishment of a diverse antigen receptor (TCR) repertoire. This observation led to current research directed at understanding how functions of B cells impact cellular immunity and regulation of immune responses in human health and disease. (3) We discovered that the TNRSF13B gene encoding a receptor (also abbreviated as TACI) expressed mostly by B cells is an immune-regulatory gene. TNRSF13B is among the most diverse gene in humans and vertebrates, TNRSF13B defines the type and intensity of innate and adaptive B cell responses, the interactions between B and T cells and in doing so also controls complement activation. Thus, while TNFRSF13B low-functioning alleles are beneficial in host defense blocking microbial transmission and epidemic spread, these same polymorphisms increase inflammation in part owing to decreasing control of complement activation. These findings suggested that TNFRSF13B gene diversity protects populations against unknown pathogens by assuring a wide array of immune responses that while disadvantageous in some individuals and in certain conditions, e.g. transplantation, will protect most against dissemination of microbes that evolved to explore the vulnerabilities of host defense. (4) We found that the fragment d of the third component of complement (C3d) markedly boosts and accelerates cellular immunity slowing and sometimes reverting progression of tumors. C3d does so by vitiating tumor induced immunosuppression, i.e. the processes that impair immune responses to tumors.
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论文共 192 篇作者统计合作学者相似作者
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Chengyi Li,Ryan Clauson,Luke F. Bugada,Fang Ke,Bing He, Zhixin Yu,Hongwei Chen, Binyamin Jacobovitz,Hongxiang Hu, Polina Chuikov,Brett Dallas Hill,Syed M. Rizvi,Yudong Song,Kai Sun, Pasieka Axenov,Daniel Huynh, Xinyi Wang,Lana Garmire,Yu Leo Lei,Irina Grigorova,Fei Wen,Marilia Cascalho,Wei Gao,Duxin Sun
I. Lei, W. Huang, H. Sicim,P. Noly, M. R. Pergande, M. C. Wilson, W. Gao, L. Liu, A. Abou, M. Jiang,S. Saddoughi, J. L. Platt,M. Cascalho, J. S. Pober, F. D. Pagani, Y. Chen, B. Pitt, Z. Wang, R. M. Mortensen, Y. Ge, P. C. Tang
JOURNAL OF HEART AND LUNG TRANSPLANTATIONno. 4 (2024): S246-S247
Results and problems in cell differentiation (2024): 213-225
Jeffrey L Platt, Chong Zhao, Jeffrey Chicca,Matthew J Pianko, Joshua Han,Stephanie The,Arvind Rao,Evan Keller,Mayara Garcia de Mattos Barbosa,Lwar Naing, Tracy Pasieka-Axenov, Lev Axenov,Simon Schaefer,Evan Farkash,Marilia Cascalho
bioRxiv the preprint server for biology (2024)
Monica Wall,Mayara Garcia de Mattos Barbosa, Natalie Hanby, Michelle Cai,Margaret Brunette, Despina Pavlidis, Paula Arrowsmith, Ansen Tan,Marilia Cascalho,Ariella Shikanov
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCESno. 6 (2024): 3431
openalex(2023)
BIOENGINEERING-BASELno. 5 (2023)
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作者统计
#Papers: 193
#Citation: 7834
H-Index: 33
G-Index: 87
Sociability: 6
Diversity: 3
Activity: 52
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