A
Aaron F. Carlin
Researcher at University of California, San Diego
Publications - 77
Citations - 6834
Aaron F. Carlin is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Medicine & Antibody. The author has an hindex of 20, co-authored 55 publications receiving 4141 citations. Previous affiliations of Aaron F. Carlin include University of Montana & University of California, Berkeley.
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Journal ArticleDOI
Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals.
Alba Grifoni,Daniela Weiskopf,Sydney I. Ramirez,Sydney I. Ramirez,Jose Mateus,Jennifer M. Dan,Jennifer M. Dan,Carolyn Rydyznski Moderbacher,Stephen A. Rawlings,Aaron Sutherland,Lakshmanane Premkumar,Ramesh Jadi,Daniel Marrama,Aravinda M. de Silva,April Frazier,Aaron F. Carlin,Jason A. Greenbaum,Bjoern Peters,Bjoern Peters,Florian Krammer,Davey M. Smith,Shane Crotty,Shane Crotty,Alessandro Sette,Alessandro Sette +24 more
TL;DR: Using HLA class I and II predicted peptide ‘megapools’, circulating SARS-CoV-2−specific CD8+ and CD4+ T cells were identified in ∼70% and 100% of COVID-19 convalescent patients, respectively, suggesting cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS.
Journal ArticleDOI
SARS-CoV-2 Infection Depends on Cellular Heparan Sulfate and ACE2.
Thomas Mandel Clausen,Thomas Mandel Clausen,Thomas Mandel Clausen,Daniel R. Sandoval,Charlotte B Spliid,Charlotte B Spliid,Charlotte B Spliid,Jessica Pihl,Jessica Pihl,Jessica Pihl,Hailee R. Perrett,Chelsea D. Painter,Anoop Narayanan,Sydney A. Majowicz,Elizabeth M. Kwong,Rachael N. McVicar,Bryan E. Thacker,Charles A. Glass,Zhang Yang,Jonathan L. Torres,Gregory J. Golden,Phillip L. Bartels,Ryan N. Porell,Aaron F. Garretson,Logan K. Laubach,Jared Feldman,Xin Yin,Yuan Pu,Blake M. Hauser,Timothy M. Caradonna,Benjamin P. Kellman,Cameron Martino,Philip L.S.M. Gordts,Sumit K. Chanda,Aaron G. Schmidt,Aaron G. Schmidt,Kamil Godula,Sandra L Leibel,Joyce Jose,Kevin D. Corbett,Andrew B. Ward,Aaron F. Carlin,Jeffrey D. Esko +42 more
TL;DR: A model in which viral attachment and infection involves heparan sulfate-dependent enhancement of binding to ACE2 is suggested, in which Manipulation of hepara sulfate or inhibition of viral adhesion by exogenous heparin presents new therapeutic opportunities.
Journal ArticleDOI
Molecular mimicry of host sialylated glycans allows a bacterial pathogen to engage neutrophil Siglec-9 and dampen the innate immune response
TL;DR: GBS can impair neutrophil defense functions by coopting a host inhibitory receptor via sialoglycan molecular mimicry, a novel mechanism of bacterial immune evasion.
Posted ContentDOI
SARS-CoV-2 Infection Depends on Cellular Heparan Sulfate and ACE2
Thomas Mandel Clausen,Daniel R. Sandoval,Charlotte B Spliid,Jessica Pihl,Hailee R. Perrett,Chelsea D. Painter,Anoop Narayanan,Sydney A. Majowicz,E. M. Kwong,Rachael N. McVicar,Bryan E. Thacker,Charles A. Glass,Zhang Yang,Jonathan L. Torres,Gregory J. Golden,Phillip L. Bartels,Ryan N. Porell,Aaron F. Garretson,Logan K. Laubach,Jared Feldman,Xin Yin,Yuan Pu,Blake M. Hauser,Timothy M. Caradonna,Benjamin P. Kellman,Cameron Martino,Gordts, Plsm, Chanda, S. K.,Aaron G. Schmidt,Kamil Godula,Sandra L Leibel,Joyce Jose,Kevin D. Corbett,Andrew B. Ward,Aaron F. Carlin,Jeffrey D. Esko +34 more
TL;DR: It is shown that SARS-CoV-2 spike protein interacts with cell surface heparan sulfate and angiotensin converting enzyme 2 (ACE2) through its Receptor Binding Domain and may represent new therapeutic opportunities for exogenous heparin.
Journal ArticleDOI
SREBP1 Contributes to Resolution of Pro-inflammatory TLR4 Signaling by Reprogramming Fatty Acid Metabolism
Yumiko Oishi,Yumiko Oishi,Nathanael J. Spann,Verena M. Link,Evan D. Muse,Tobias Strid,Chantle Edillor,Matthew J. Kolar,Takashi Matsuzaka,Sumio Hayakawa,Jenhan Tao,Minna U. Kaikkonen,Aaron F. Carlin,Michael T. Lam,Ichiro Manabe,Hitoshi Shimano,Alan Saghatelian,Christopher K. Glass +17 more
TL;DR: It is shown that SREBP1 contributes to the resolution phase of TLR4-induced gene activation by reprogramming macrophage lipid metabolism and results in the uncoupling of NFκB binding from gene activation.