Robert B. Ratts
University of Texas Southwestern Medical Center
8 Papers
143 Citations
Robert B. Ratts is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Cytotoxic T cell & T cell. The author has an hindex of 6, co-authored 8 publications.
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Papers
Silencing T-bet Defines a Critical Role in the Differentiation of Autoreactive T Lymphocytes
Amy E. Lovett-Racke,Anne E. Rocchini,Judy Choy,Sara C. Northrop,Rehana Z. Hussain,Robert B. Ratts,Devanjan Sikder,Michael K. Racke +7 more
TL;DR: T-bet was shown to bind the IFNgamma and STAT1 promoters, but did not regulate the IL-12/STAT4 pathway, which means T-bet may be a target for therapeutics for Th1-mediated diseases.
199
•Journal Article
Blockade of CD28 during in vitro activation of encephalitogenic T cells or after disease onset ameliorates experimental autoimmune encephalomyelitis.
TL;DR: It is found that CD28 blockade ameliorated EAE during the efferent and afferent limbs of the immune response and suggested a clinically relevant therapeutic scenario for human diseases, such as multiple sclerosis.
126
Phenotypic characterization of autoreactive T cells in multiple sclerosis
Robert B. Ratts,Nitin J. Karandikar,Rehana Z. Hussain,Judy Choy,Sara C. Northrop,Amy E. Lovett-Racke,Michael K. Racke +6 more
TL;DR: This report examined myelin-specific CD8 and CD4 T cells for two markers differentially expressed on naïve, memory and chronically stimulated T cells, CD28 and CD57, and observed differential expression on CD8 T cells in response to myelin antigens, but not in response the recall antigen mumps.
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CD28-CD57+ T cells predominate in CD8 responses to glatiramer acetate.
Robert B. Ratts,Amy E. Lovett-Racke,Judy Choy,Sara C. Northrop,Rehana Z. Hussain,Nitin J. Karandikar,Michael K. Racke +6 more
TL;DR: Employing MS patients before and after chronic in vivo administration of the antigen glatiramer acetate (GA) to examine this hypothesis that human T cells adopt a CD28-CD57+ phenotype in chronic viral infections, this phenotype was only observed after chronic stimulation and not in a recall response to mumps.
17
The Role of Costimulation in Experimental Autoimmune Encephalomyelitis
Michael K. Racke,Robert B. Ratts,Rodney W. Stuart,Caishu Deng,Amy E. Lovett-Racke +4 more
- 01 Jan 2005
TL;DR: It appears the costimulation provided by B7-1 is important in disease development, while B8-2 may play an important regulatory role, and other costimulatory pathways, such as CD40/CD40L and ICOS and its ligand, also play significant roles in the EAE model.