Robert Modlin*

Robert L Modlin

Professor, Medicine, University of California Los Angeles

Professor, MIMG, University of California Los Angeles

(310) 917-3376

Laboratory Address:
BSRB 210B

Work Address:
615 Charles E. Young South
210B BSRB
Los Angeles, CA 90095

Affiliations

Chief and Professor, Dermatology
Member, CTSI, California NanoSystems Institute, Immunity, Microbes & Molecular Pathogenesis GPB Home Area, Tumor Immunology Program at the Jonsson Comprehensive Cancer Center (JCCC)
 

Research Interests

Infectious disease poses a major health problem worldwide. Essential to control of these diseases is the elucidation of mechanisms by which the innate and adaptive immune systems defend against microbial pathogens. We have investigated human immune responses in the context of two major human infectious diseases, leprosy and tuberculosis. Our studies provided new paradigms for human innate immune responses including the first evidence that Toll-like receptors recognize microbial lipoproteins and can activate macrophages to kill intracellular pathogens. Our work revealed that humans and mice have evolved distinct antimicrobial pathways in their innate immune systems, and demonstrated a novel vitamin D-dependent pathway in human macrophages that generates antimicrobial peptides, e.g. cathelicidin, that kill intracellular pathogens, including M. tuberculosis. Macrophage antimicrobial and phagocytic programs were shown to be differentially programmed by the innate system via IL-15 and IL-10 respectively, which impact the outcome of microbial infection. Our lab has also described new paradigms for human acquired immunity by demonstrating: distinct Th1 and Th2 cytokine patterns in disease lesions of different clinical forms of human leprosy; similar utilization of the common vitamin D-dependent and antimicrobial peptide pathway, and differential regulation of this activity by different cytokines. Since vitamin D is synthesized in response to UV light, these studies have provided novel insights into the known differential susceptibility to microbial pathogens of humans of African and Asian descent and suggested new approaches to translational intervention to enhance immunity. These discoveries were made through study of human leprosy and tuberculosis, ancient diseases caused by intracellular pathogens that still pose major health and economic burdens to developing countries.
 

Biography

Robert L. Modlin, M.D. is Chief, Division of Dermatology, and Professor of Dermatology, Department of Medicine and Department of Microbiology, Immunology and Molecular Genetics, at the David Geffen School of Medicine at UCLA. He received his medical degree form New York University and residency training from Los Angeles County/ University of Southern California Medical Center.

Dr. Modlin’s lab is interested in the immunology of microbial infection. Infectious disease poses a major health problem worldwide. Essential to control of these diseases is the elucidation of immune mechanisms that result in resistance versus susceptibility to infection. The laboratory’s focus is the identification of novel mechanisms by which the innate and adaptive immune system combat microbial pathogens. Using leprosy as a model, Dr. Modlin’s lab has made important contributions to our understanding of immunology including the role of mammalian Toll-like receptors and CD1-restricted T cells in host defense, including the cytokines pattens and antimicrobial pathways. These studies include 3 papers published in Nature and 10 in Science. It is hoped that the insights obtained from these studies will lead to better treatments and prevention of infectious diseases in humans.

Publications