Dr. David M. Center MD
Pulmonologist | Pulmonary Disease
725 Albany Street Shapiro, Suite B Boston MA, 02118About
Dr. David Center practices Pulmonology in Boston, MA. A pulmonologist is a physician who possesses specialized knowledge and skill in the diagnosis and treatment of pulmonary conditions and diseases. Dr. Center manages patients who need life support and mechanical ventilation, and is specially trained in diseases and conditions of the chest, particularly pneumonia, asthma, tuberculosis, emphysema, and complicated chest infections.
Education and Training
Boston University School of Medicine 1972
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM- Pulmonary Disease
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Histamine h(4) and h(2) receptors control histamine-induced interleukin-16 release from human CD8(+) T cells.
- Prointerleukin-16 contains a functional CcN motif that regulates nuclear localization.
- Tumor necrosis factor-alpha-induced synthesis of interleukin-16 in airway epithelial cells: priming for serotonin stimulation.
- Binding of HTLV-1 tax oncoprotein to the precursor of interleukin-16, a T cell PDZ domain-containing protein.
- Immunomodulatory effect of interleukin-16 on allergic airway inflammation.
- Induced sputum analysis for T helper type 2 cell regulation: closing the loop.
- Immunomodulatory cytokines in asthmatic inflammation.
- Cutting edge: IL-16/CD4 preferentially induces Th1 cell migration: requirement of CCR5.
- Nuclear pro-IL-16 regulation of T cell proliferation: p27(KIP1)-dependent G0/G1 arrest mediated by inhibition of Skp2 transcription.
- The effect of interleukin-16 and its precursor on T lymphocyte activation and growth.
- Regulation of nuclear Prointerleukin-16 and p27(Kip1) in primary human T lymphocytes.
- Chemokine receptor CXCR3 desensitization by IL-16/CD4 signaling is dependent on CCR5 and intact membrane cholesterol.
- Taking the "idio" out of idiopathic pulmonary fibrosis: a call to arms.
- Histamine 4 receptor activation induces recruitment of FoxP3+ T cells and inhibits allergic asthma in a murine model.
- Pro-IL-16 recruits histone deacetylase 3 to the Skp2 core promoter through interaction with transcription factor GABP.
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