- ASSISTANT PROFESSOR Medicine, Pulmonary, Critical Care and Sleep Medicine
Critical Care Medicine
American Board of Internal Medicine
MD, Medizinische Hochschule Hannover
Residency, Internal Medicine
Albert Einstein Medical Center
Fellowship, Pulmonary & CC Med
Mount Sinai Hospital
- Dr. Christian Becker received combined MD (1999) and PhD degrees (2001, molecular genetics) from Hannover Medical School in Germany. He trained in Internal Medicine in Germany (2000-2002) and subsequently in the US (2002-2005), followed by clinical (2005-2008) and research fellowship training (2008-2009) in Pulmonary and Critical Care Medicine. He joined the faculty of Mount Sinai School of Medicine in 2009 as a physician scientist with a translational research focus on human lung dendritic cell anatomic and functional diversity in the steady state and pulmonary disease, specifically idiopathic pulmonary fibrosis (IPF) and sarcoidosis. In addition, Dr. Becker is involved in various immunophenotyping studies: he is the principal investigator for a clinical study on myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS), which is examining the effects of physical exercise on the immune status of patients with this condition, and is conducting immunophenotyping studies on sarcoidosis and IPF.
He continues to see patients in both outpatient and inpatient settings.
Outstanding Medical Educator Award
Icahn School of Medicine at Mount Sinai
Faculty Excellence in Teaching Award
Pulmonary and Critical Care Fellowship Program
Roche Postdoctoral Fellowship Award
2011 - 2013
Faculty Training Grant Award in Cancer Biology
National Cancer Institute
American College of Chest Physicians (ACCP)
Outstanding Graduating Resident Award
Albert Einstein Medical Center, Philadelphia, PA
PhD thesis awarded 'Summa Cum Laude'
Medizinische Hochschule Hannover
Idiopathic Pulmonary Fibrosis (IPF)
Idiopathic pulmonary fibrosis (IPF) is a chronically progressive, irreversible and ultimately fatal fibrosing lung disease. The disease affects many patients worldwide without any geographical or racial predilection. The prevalence in the US is estimated at around 20 cases per 100,000 for males and 13 cases per 100,000 for females. The disease imposes both a high symptom burden and an ultimately fatal prognosis on affected patients and their families. The median survival time after diagnosis currently is only 2.5 to 3.5 years. Our understanding of this disease, its cause(s) and underlying pathogenetic mechanisms is poor. There is no effective treatment available to date. Secondary forms ofpulmonary fibrosis affect a much higher number of patients, but exact numbers on prevalence, morbidity and mortality are difficult to estimate given the heterogeneity of the different underlying conditions. A characterization of how the different dendritic cell subsets are dysfunctional in pulmonary fibrosis will help to better understand the underlying pathogenetic mechanisms and may offer new insights into therapeutic options to halt the progression of the fibrotic remodeling process in patients afflicted with this condition.
Human Lung Dendritic Cell Anatomic and Functional Diversity
The respiratory tract is one of the organ systems in the human body directly confronted with the outside world, making effective immune surveillance and defense mechanisms essential. Dendritic cells (DCs) are emerging as prominent regulators of immune responses in the lung. Historically, a large body of work has looked into the anatomic and functional properties of DCs in the respiratory system. Recent studies utilizing novel research techniques are rapidly expanding our knowledge. Most of this recent work has been done using animal models. We are characterizing the phenotypes of dendritic cells in the normal human lung and in disease states in which dendritic cells are either proven or implicated to play important roles in pathogenesis and pathophysiology, namely, but not limited to, sarcoidosis and idiopathic as well as secondary forms of pulmonary fibrosis.
SarcoidosisSarcoidosis is a systemic granulomatous disease that prominently affects the lungs in almost all cases. There are multiple studies suggesting an interesting functional role of dendritic cells in this disease, which – together with the fact that our medical center is a longstanding center of excellence in sarcoidosis research and a regional referral center for patients with the whole spectrum of clinical disease phenotypes - makes it a prime candidate to assess the different DC subpopulations in affected human lung and locoregionary lymph node tissue and to correlate the findings with the various different disease phenotypes we see at Mount Sinai (resolving disease vs. chronically progressive or fibrosing disease).
Agudo J, Ruzo A, Tung N, Salmon H, Leboeuf M, Hashimoto D, Becker C, Garrett-Sinha L, Baccarini A, Merad M, Brown B. The miR-126–VEGFR2 axis controls the innate response to pathogen-associated nucleic acids. Nature Immunology 2014; 15: 54-62.
Hashimoto D, Chow A, Noizat C, Teo P, Beasley MB, Leboeuf M, Becker CD, See P, Price J, Lucas D, Greter M, Mortha A, Boyer SW, Forsberg EC, Tanaka M, van Rooijen N, García-Sastre A, Stanley ER, Ginhoux F, Frenette PS, Merad M. Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes. Immunity 2013 Apr; 38(4).
Yu CI, Becker C, Wang Y, Marches F, Helft J, Leboeuf M, Anguiano E, Pourpe S, Goller K, Pascual V, Banchereau J, Merad M, Palucka K. Human CD1c+ dendritic cells drive the differentiation of CD103+ CD8+ mucosal effector T cells via the cytokine TGF-β. Immunity 2013 Apr; 38(4).
Stanke F, Becker T, Kumar V, Hedtfeld S, Becker C, Cuppens H, Tamm S, Yarden J, Laabs U, Siebert B, Fernandez L, Macek M, Radojkovic D, Ballmann M, Greipel J, Cassiman JJ, Wienker TF, Tümmler B. Genes that determine immunology and inflammation modify the basic defect of impaired ion conductance in cystic fibrosis epithelia. Journal of medical genetics 2011 Jan; 48(1).
Becker C, Teirstein AS. Comment: The anergic state in sarcoidosis is associated with diminished dendritic cell function. Journal of immunology (Baltimore, Md. : 1950) 2009 Apr; 182(7).
Becker C, Sridhar P, Iannuzzi MC. Cardiac sarcoidosis associated with BTNL2. Cardiology 2009; 112(1).
Becker C, Gil J, Padilla ML. Idiopathic pleuroparenchymal fibroelastosis: an unrecognized or misdiagnosed entity?. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 2008 Jun; 21(6).
Becker C, Fischer RA. Acute cholecystitis caused by ceftriaxone stones in an adult. Case reports in medicine 2009; 2009.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr. Becker did not report having any of the following types of financial relationships with industry during 2012 and/or 2013: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.
Guggenheim Pavilion Floor 5W Room 131
1190 Fifth Avenue
New York, NY 10029
Guggenheim Pavilion Floor 5W Room 131
1190 Fifth Avenue
New York, NY 10029