What is he best known for?
The fields of study he is best known for:
- Gene
- Immune system
- Cytokine
His scientific interests lie mostly in Immunology, Arthritis, Type II collagen, FOXP3 and T cell.
He combines subjects such as Autoimmune disease, Antibody and B cell with his study of Arthritis.
David D. Brand has included themes like Glutaraldehyde, Molecular biology, Rheumatoid arthritis and Carbodiimide in his Type II collagen study.
David D. Brand interconnects Adjuvant, Immunization, Cyanogen bromide and Disease in the investigation of issues within Rheumatoid arthritis.
His FOXP3 research includes elements of Cell, IL-2 receptor, Cellular differentiation, Transforming growth factor beta and Retinoic acid.
David D. Brand studied T cell and Major histocompatibility complex that intersect with Immunodominance.
His most cited work include:
- Collagen-induced arthritis (728 citations)
- Collagen-induced arthritis (728 citations)
- IL-17–dependent cellular immunity to collagen type V predisposes to obliterative bronchiolitis in human lung transplants (339 citations)
What are the main themes of his work throughout his whole career to date?
David D. Brand focuses on Immunology, Arthritis, Type II collagen, T cell and FOXP3.
Immunology is closely attributed to In vivo in his study.
He has researched Arthritis in several fields, including Molecular biology, Cytokine, Autoimmune disease and Recombinant DNA.
His biological study deals with issues like Biochemistry, which deal with fields such as Biophysics.
His FOXP3 research is multidisciplinary, relying on both Cell, Cancer research, IL-2 receptor, Cell biology and Transforming growth factor beta.
The study incorporates disciplines such as Inflammation, Disease and Transgene in addition to Rheumatoid arthritis.
He most often published in these fields:
- Immunology (75.00%)
- Arthritis (69.29%)
- Type II collagen (39.29%)
What were the highlights of his more recent work (between 2013-2021)?
- Immunology (75.00%)
- Arthritis (69.29%)
- Internal medicine (20.00%)
In recent papers he was focusing on the following fields of study:
Immunology, Arthritis, Internal medicine, T cell and Cell biology are his primary areas of study.
His study focuses on the intersection of Immunology and fields such as Cytotoxic T cell with connections in the field of Peptide binding and Major histocompatibility complex.
His study in the fields of Type II collagen under the domain of Arthritis overlaps with other disciplines such as Congenic breeding.
His studies in Type II collagen integrate themes in fields like Extracellular matrix and In vivo.
His work in Internal medicine addresses issues such as Endocrinology, which are connected to fields such as Angiotensin II and Angiotensin receptor.
His work on T-cell receptor as part of general T cell research is frequently linked to Syk, bridging the gap between disciplines.
Between 2013 and 2021, his most popular works were:
- Critical role of all-trans retinoic acid in stabilizing human natural regulatory T cells under inflammatory conditions (142 citations)
- Role of TNF-TNF Receptor 2 Signal in Regulatory T Cells and Its Therapeutic Implications (88 citations)
- Role of Vitamin A in the Immune System. (84 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Immune system
- Cytokine
The scientist’s investigation covers issues in Immunology, Cell biology, FOXP3, Cellular differentiation and Cancer research.
His Immunology study combines topics in areas such as Periodontal disease and Rheumatology.
His Cell biology study incorporates themes from Tissue engineering, In vitro and Type II collagen.
The various areas that David D. Brand examines in his FOXP3 study include Transforming growth factor beta, Tretinoin, Retinoic acid and CD8.
The concepts of his Cellular differentiation study are interwoven with issues in Autoantibody, Autoimmunity, B-cell activating factor and Immunoglobulin class switching.
His Cancer research research incorporates themes from Biomarker, Downregulation and upregulation, Long non-coding RNA and Tumor necrosis factor alpha.
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