Muzlifah Haniffa

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Muzlifah Haniffa
Professor Muzlifah Haniffa presenting at a 2020 conference (cropped).jpg
Presenting at the Wellcome Trust Sanger Institute in 2020
Born
Penang, Malaysia
Alma materNewcastle University
Scientific career
FieldsDermatology, Immunology, Bioinformatics

Muzlifah Haniffa is a Malaysian dermatologist and immunologist who focuses on the development of the immune system and the use of single-cell techniques to understand biology. Haniffa is a professor and Wellcome Trust Senior Research Fellow in the Faculty of Medical Sciences at Newcastle University. [1] [2]

Contents

Early life and education

Haniffa was born in Penang, Malaysia. [3] Her interests in science as a child were piqued initially by space, but later she decided to pursue a career as a clinical scientist. [2] Haniffa studied at Tunku Kurshiah College, Seremban and moved to the UK in the 1990s. [4] Haniffa graduated BSc, MBBCh from the University of Wales College of Medicine in 1999. She became a member of the Royal College of Physicians in 2002. In 2007, she earned a diploma in epidemiology from the London School of Hygiene & Tropical Medicine. [1] She completed her PhD from Newcastle University in 2009 and completed her clinical dermatology training in 2010. [1] She was runner-up for the 2009 Sue McCarthy Prize from the Medical Research Council. [1]

Career

In 2013 the European Society for Dermatology Research awarded Haniffa a Silver Award for her research. [1] She was shortlisted for the 2016 North Eastern Woman Entrepreneur of the Year awards in the STEM category. [5] In 2016 her research into the functions of white blood cells was boosted by a £200,000 fellowship by the Lister Institute of Preventive Medicine. [3] [2] [4] Professor Chris Day, serving as vice-chancellor of the medical faculty, congratulated Haniffa on her achievement, saying: [4]

Professor Haniffa is one of the outstanding clinician scientists of her generation and has rapidly, in her short career, established an international reputation in her field

Chris Day

Haniffa's work on the immune system has included discovering that a population of what was considered dendritic cells (defined by the presence of CD14) in human skin were in fact macrophages, and studies demonstrating that a subset of dendritic cells exist in mice which can activate T helper 17 cells against a fungal infection. [6] [7] Haniffa was awarded the 2018 Early Career Prize in Allerlology by the 5th European Congress on Immunology. [8]

Haniffa is a member of the Human Cell Atlas, which aims to characterise all cells in the human body using single-cell transcriptomic techniques, alongside Sarah Teichmann, Fiona Powrie, Ashley Moffett, and others. [9] [10] [11] In 2018 her lab contributed to the discovery of the major subset of kidney cells which become mutated and give rise to kidney cancers. This was accomplished by matching the biological make-up of kidney carcinoma cells to given healthy kidney cells. [12] [13] [14] This was followed by a single-cell study of the placenta which discovered new cell sub-types in the decidua, informing understanding of how the maternal and fetal immune systems interact with each other and avoid miscarriage or pre-eclampsia. [15] [16] [17] The study used 70,000 cells and tissue from the Human Developmental Biology Resource. [15] In addition Haniffa and collaborators have published single-cell studies on the innate and adaptive immune system, including regulatory T cells, dendritic cells, and monocytes. [18] [19] [20] [21] In 2019 the Chan Zuckerberg Initiative announced that it was investing $68 million in grants into furthering the Human Cell Atlas, including awards for Haniffa to study the immune system and liver during ageing in single-cell detail. [22] [23] [24]

She is a committee member of the British Society for Investigative Dermatology, who had awarded Haniffa a Junior Investigator Prize in 2012. [1] [25]

Related Research Articles

<span class="mw-page-title-main">Dendritic cell</span> Accessory cell of the mammalian immune system

A dendritic cell (DC) is an antigen-presenting cell of the mammalian immune system. A DC's main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and adaptive immune systems.

<span class="mw-page-title-main">Phagocyte</span> Cells that ingest harmful matter within the body

Phagocytes are cells that protect the body by ingesting harmful foreign particles, bacteria, and dead or dying cells. Their name comes from the Greek phagein, "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek kutos, "hollow vessel". They are essential for fighting infections and for subsequent immunity. Phagocytes are important throughout the animal kingdom and are highly developed within vertebrates. One litre of human blood contains about six billion phagocytes. They were discovered in 1882 by Ilya Ilyich Mechnikov while he was studying starfish larvae. Mechnikov was awarded the 1908 Nobel Prize in Physiology or Medicine for his discovery. Phagocytes occur in many species; some amoebae behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.

<span class="mw-page-title-main">Monocyte</span> Subtype of leukocytes

Monocytes are a type of leukocyte or white blood cell. They are the largest type of leukocyte in blood and can differentiate into macrophages and monocyte-derived dendritic cells. As a part of the vertebrate innate immune system monocytes also influence adaptive immune responses and exert tissue repair functions. There are at least three subclasses of monocytes in human blood based on their phenotypic receptors.

<span class="mw-page-title-main">Langerhans cell</span> Cell type

A Langerhans cell (LC) is a tissue-resident macrophage of the skin once thought to be a resident dendritic cell. These cells contain organelles called Birbeck granules. They are present in all layers of the epidermis and are most prominent in the stratum spinosum. They also occur in the papillary dermis, particularly around blood vessels, as well as in the mucosa of the mouth, foreskin, and vaginal epithelium. They can be found in other tissues, such as lymph nodes, particularly in association with the condition Langerhans cell histiocytosis (LCH).

<span class="mw-page-title-main">Macrophage inflammatory protein</span> Protein family

Macrophage Inflammatory Proteins (MIP) belong to the family of chemotactic cytokines known as chemokines. In humans, there are two major forms, MIP-1α and MIP-1β that are now officially named CCL3 and CCL4, respectively. However, other names can sometimes be encountered, especially in older literature, as LD78α, AT 464.1 and GOS19-1 for human CCL3 and AT 744, Act-2, LAG-1, HC21 and G-26 for human CCL4. Other macrophage inflammatory proteins include MIP-2, MIP-3 and MIP-5.

<span class="mw-page-title-main">Monoblast</span>

Monoblasts are the committed progenitor cells that differentiated from a committed macrophage or dendritic cell precursor (MDP) in the process of hematopoiesis. They are the first developmental stage in the monocyte series leading to a macrophage. Their myeloid cell fate is induced by the concentration of cytokines they are surrounded by during development. These cytokines induce the activation of transcription factors which push completion of the monoblast's myeloid cell fate. Monoblasts are normally found in bone marrow and do not appear in the normal peripheral blood. They mature into monocytes which, in turn, develop into macrophages. They then are seen as macrophages in the normal peripheral blood and many different tissues of the body. Macrophages can produce a variety of effector molecules that initiate local, systemic inflammatory responses. These monoblast differentiated cells are equipped to fight off foreign invaders using pattern recognition receptors to detect antigen as part of the innate immune response.

A complement receptor is a membrane-bound receptor belonging to the complement system, which is part of the innate immune system. Complement receptors bind effector protein fragments that are produced in response to antigen-antibody complexes or damage-associated molecules. Complement receptor activation contributes to the regulation of inflammation, leukocyte extravasation, and phagocytosis; it also contributes to the adaptive immune response. Different complement receptors can participate in either the classical complement pathway, the alternative complement pathway, or both.

<span class="mw-page-title-main">CX3C motif chemokine receptor 1</span> Protein-coding gene in the species Homo sapiens

CX3C motif chemokine receptor 1 (CX3CR1), also known as the fractalkine receptor or G-protein coupled receptor 13 (GPR13), is a transmembrane protein of the G protein-coupled receptor 1 (GPCR1) family and the only known member of the CX3C chemokine receptor subfamily.

<span class="mw-page-title-main">CD83</span>

CD83 is a human protein encoded by the CD83 gene.

<span class="mw-page-title-main">CLEC10A</span> Protein-coding gene in the species Homo sapiens

C-type lectin domain family 10 member A (CLEC10A) also designated as CD301 is a protein that in humans is encoded by the CLEC10A gene. CLEC10A is part of the C-type lectin superfamily and binds to N-Acetylgalactosamine (GalNAc). It is mainly expressed on myeloid cells and also on oocytes and very early stages of embryogenesis. CLEC10A is used as a marker of the CD1c+ dendritic cell subgroup, also called cDC2. The actions of CLEC10A are diverse, depending on the ligand and environment.

<span class="mw-page-title-main">Aviv Regev</span> Bioinformatician

Aviv Regev is a computational biologist and systems biologist and Executive Vice President and Head of Genentech Research and Early Development in Genentech/Roche. She is a core member at the Broad Institute of MIT and Harvard and professor at the Department of Biology of the Massachusetts Institute of Technology. Regev is a pioneer of single cell genomics and of computational and systems biology of gene regulatory circuits. She founded and leads the Human Cell Atlas project, together with Sarah Teichmann.

<span class="mw-page-title-main">Dana Pe'er</span> Bioinformatician

Dana Pe'er, Chair and Professor in Computational and Systems Biology Program at Sloan Kettering Institute is a researcher in computational systems biology. A Howard Hughes Medical Institute (HHMI) Investigator since 2021, she was previously a professor at Columbia Department of Biological Sciences. Pe'er's research focuses on understanding the organization, function and evolution of molecular networks, particularly how genetic variations alter the regulatory network and how these genetic variations can cause cancer.

The dendritic cell-based cancer vaccine is an innovation in therapeutic strategy for cancer patients.

Dipyaman Ganguly is an Indian physician-scientist immunologist and cell biologist, currently a Principal Scientist and Swarnajayanthi Fellow at the CSIR-Indian Institute of Chemical Biology (IICB). He heads the Dendritic Cell Laboratory of IICB, popularly known as the Ganguly Lab, where he hosts several researchers involved in research on regulation of innate Immunity and pathogenesis of inflammatory disorders. The Council of Scientific and Industrial Research, the apex agency of the Government of India for scientific research, awarded him the Shanti Swarup Bhatnagar Prize for Science and Technology, one of the highest Indian science awards for his contributions to Medical Sciences in 2022.

Miram Merad is a French-Algerian professor in Cancer immunology and the Director of the Marc and Jennifer Lipschultz Precision Immunology Institute (PrIISM) at the Icahn School of Medicine at Mount Sinai (ISMMS) in New York, NY. She is the corecipient of the 2018 William B. Coley Award for Distinguished Research in Basic Immunology and a member of the United States National Academy of Sciences and the National Academy of Medicine.

The Human Cell Atlas is a project to describe all cell types in the human body. The initiative was announced by a consortium after its inaugural meeting in London in October 2016, which established the first phase of the project. Aviv Regev and Sarah Teichmann defined the goals of the project at that meeting, which was convened by the Broad Institute, the Wellcome Trust Sanger Institute and Wellcome Trust. Regev and Teichmann lead the project.

<span class="mw-page-title-main">Gwendalyn J. Randolph</span> American immunologist

Gwendalyn J. Randolph is an American immunologist, the Emil R. Unanue Distinguished Professor in the Department of Immunology and Pathology at Washington University School of Medicine where she is currently co-director of the Immunology Graduate Program. During her postdoctoral work, Randolph characterized monocyte differentiation to dendritic cells and macrophages and made advances in our understanding of dendritic cell trafficking and the fate of monocytes recruited to sites of inflammation. Her lab has contributed to the Immunological Genome Project by characterizing macrophage gene expression. Her work now focuses on the immunological mechanisms driving atherosclerosis and inflammatory bowel disease (IBD) by exploring lymphatic function and lipoprotein trafficking.

<span class="mw-page-title-main">Dermal macrophage</span> Skin macrophages used for wound repair and hair growth

Dermal macrophages are macrophages in the skin that facilitate skin homeostasis by mediating wound repair, hair growth, and salt balance. Their functional role in these processes is the mediator of inflammation. They can acquire an M1 or M2 phenotype to promote or suppress an inflammatory response, thereby influencing other cells' activity via the production of pro-inflammatory or anti-inflammatory cytokines. Dermal macrophages' ability to acquire pro-inflammatory properties also potentiates them in cancer defence. M1 macrophages can suppress tumour growth in the skin by their pro-inflammatory properties. However, M2 macrophages support tumour growth and invasion by the production of Th2 cytokines such as TGFβ and IL-10. Thus, the exact contribution of each phenotype to cancer defence and the skin's homeostasis is still unclear.

Menna R. Clatworthy FRCP FMedSci FLSW is a British immunologist who is Professor of Translational Medicine at the University of Cambridge. She studies human tissue immunity. She is a Fellow of the Academy of Medical Sciences and was elected to the European Molecular Biology Organization in 2022.

Jasmin Fisher, is an Israeli-British biologist who is Professor of computational biology at University College London. She is Group Leader of the Fisher Lab at UCL Cancer Institute, which develops state-of-the-art computational models and analysis techniques to study cancer evolution and mechanisms of drug resistance to identify better personalised treatments for cancer patients.

References

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