Professor, University of Massachusetts Medical School
Rheumatology
Dr. Samuel M. Behar, MD
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Doctor Samuel M. Behar, MD is an expert in the field of Rheumatology. He attended Albert Einstein College of Medicine of Yeshiva University. Dr. Samuel M. Behar is a published doctor. He published 57 publications, including: 'TIM3 Mediates T Cell Exhaustion during Mycobacterium tuberculosis Infection.'
Publications
- Multiple Inflammatory Cytokines Converge To Regulate CD8+ T Cell Expansion and Function during Tuberculosis.
- Orchestration of pulmonary T cell immunity during Mycobacterium tuberculosis infection: Immunity interruptus.
- Chromatin Decondensation and T Cell Hyperresponsiveness in Diabetes-Associated Hyperglycemia.
- Immunology: Fixing the odds against tuberculosis.
- In search of a new paradigm for protective immunity to TB.
- Macrophages clean up: efferocytosis and microbial control.
- iNKT Cell Production of GM-CSF Controls Mycobacterium tuberculosis.
- Tryptophan biosynthesis protects mycobacteria from CD4 T-cell-mediated killing.
- Antigen-specific CD8(+) T cells and protective immunity to tuberculosis.
- IL-1? Promotes Antimicrobial Immunity in Macrophages by Regulating TNFR Signaling and Caspase-3 Activation.
- Recognition of microbial and mammalian phospholipid antigens by NKT cells with diverse TCRs.
- Efferocytosis is an innate antibacterial mechanism.
- A Comparative Lipidomics Platform for Chemotaxonomic Analysis of Mycobacterium tuberculosis.
- Regulation of neutrophils by interferon-{gamma} limits lung inflammation during tuberculosis infection.
- Emerging Tim-3 functions in antimicrobial and tumor immunity.
- Requirement for Invariant chain in macrophages for Mycobacterium tuberculosis replication and CD1d antigen presentation.
- Critical role for invariant chain in CD1d-mediated selection and maturation of Vα14-invariant NKT cells.
- Development of a Glycoprotein D-Expressing Dominant-Negative and Replication-Defective Herpes Simplex Virus 2 (HSV-2) Recombinant Viral Vaccine against HSV-2 Infection...
- Cardiolipin Binds to CD1d and Stimulates CD1d-Restricted {gamma}{delta} T Cells in the Normal Murine Repertoire.
- Lipids, apoptosis, and cross-presentation: links in the chain of host defense against Mycobacterium tuberculosis.
- Mycobacterium tuberculosis directs immunofocusing of CD8+ T cell responses despite vaccination.
- Tim3 binding to galectin-9 stimulates antimicrobial immunity.
- Alpha-galactosylceramide as a therapeutic agent for pulmonary Mycobacterium tuberculosis infection.
- Primary deficiency of microsomal triglyceride transfer protein in human abetalipoproteinemia is associated with loss of CD1 function.
- Eicosanoid pathways regulate adaptive immunity to Mycobacterium tuberculosis.
- Synovial fibroblasts self-direct multicellular lining architecture and synthetic function in three-dimensional organ culture.
- EspA acts as a critical mediator of ESX1-dependent virulence in Mycobacterium tuberculosis by affecting bacterial cell wall integrity.
- Vaccine-induced antibody isotypes are skewed by impaired CD4 T cell and invariant NKT cell effector responses in MyD88-deficient mice.
- Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair.
- Mycobacterium tuberculosis-specific CD8+ T cells require perforin to kill target cells and provide protection in vivo.
- Innate invariant NKT cells recognize Mycobacterium tuberculosis-infected macrophages, produce interferon-gamma, and kill intracellular bacteria.
- Lipid mediators in innate immunity against tuberculosis: opposing roles of PGE2 and LXA4 in the induction of macrophage death.
- Tuberculosis triggers a tissue-dependent program of differentiation and acquisition of effector functions by circulating monocytes.
- Mycolyltransferase-mediated glycolipid exchange in Mycobacteria.
- Bacterial protein secretion is required for priming of CD8+ T cells specific for the Mycobacterium tuberculosis antigen CFP10.
- Discordant QuantiFERON-TB Gold test results among US healthcare workers with increased risk of latent tuberculosis infection: a problem or solution?
- Vaccine-elicited 10-kilodalton culture filtrate protein-specific CD8+ T cells are sufficient to mediate protection against Mycobacterium tuberculosis infection.
- Antigen-specific CD8+ T cells and the development of central memory during Mycobacterium tuberculosis infection.
- Natural killer T cells recognize diacylglycerol antigens from pathogenic bacteria.
- The LFA-1 adhesion molecule is required for protective immunity during pulmonary Mycobacterium tuberculosis infection.
- Mycobacterium tuberculosis-specific CD8+ T cells and their role in immunity.
- Interplay of cytokines and microbial signals in regulation of CD1d expression and NKT cell activation.
- Anamnestic responses of mice following Mycobacterium tuberculosis infection.
- In vivo depletion of CD11c+ cells delays the CD4+ T cell response to Mycobacterium tuberculosis and exacerbates the outcome of infection.
- Primary type II alveolar epithelial cells present microbial antigens to antigen-specific CD4+ T cells.
- Cytolytic CD8+ T cells recognizing CFP10 are recruited to the lung after Mycobacterium tuberculosis infection.
- The major histocompatibility complex haplotype affects T-cell recognition of mycobacterial antigens but not resistance to Mycobacterium tuberculosis in C3H mice.
- Structural features of the acyl chain determine self-phospholipid antigen recognition by a CD1d-restricted invariant NKT (iNKT) cell.
- Lysosomal localization of murine CD1d mediated by AP-3 is necessary for NK T cell development.
- Role of CD1d-restricted NKT cells in microbial immunity.
- Toll-like receptor 4-defective C3H/HeJ mice are not more susceptible than other C3H substrains to infection with Mycobacterium tuberculosis.
- Conservation of CD1 intracellular trafficking patterns between mammalian species.
- Activation of NKT cells protects mice from tuberculosis.
- Dissemination of Mycobacterium tuberculosis is influenced by host factors and precedes the initiation of T-cell immunity.
- Fine specificity of TCR complementarity-determining region residues and lipid antigen hydrophilic moieties in the recognition of a CD1-lipid complex.
- TIM3 Mediates T Cell Exhaustion during Mycobacterium tuberculosis Infection.
Schools
Albert Einstein College of Medicine of Yeshiva University
Doctors Specialties
- Rheumatology
Accepted Insurances
Education
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Brigham and Women's Hospital -
Albert Einstein College of Medicine of Yeshiva University
Hospital
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Brigham and Women's Hospital
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