Jane Howard

Jane Howard


  • Reader of Endocrinology & Diabetes, SCMMS Guys
    • 9668

    Personal profile

    Research interests

    My research focuses on immune-endocrine interactions. We were the first to report that the adipocyte-derived hormone leptin, a key regulator of food intake and energy homeostasis, is also an important immune-modulatory cytokine linking nutritional status with immune function (Nature 1998, JCI 1999). Further work in the Flier Lab at Harvard investigated the role of suppressor of cytokine signalling 3 as a potential molecular mediator of leptin resistance (Nature Medicine 2004, Cell Metabolism 2006). I have continued and developed my interest in immunometabolism at KCL.

    The close association between nutrient excess and alterations in the cellular and molecular mediators of inflammation and immunity is being increasingly appreciated, particularly in the development of obesity and insulin resistance. 

    Both type 2 diabetes and obesity are characterized by a low-grade inflammatory state. Alteration of immune cell subpopulations in adipose tissue is a major part of this process. Early studies examined the role of adipose tissue macrophages in obesity, but recent reports suggest a key role of the adaptive immune system. Adipose tissue (AT)-associated T cells have been proposed to play an important role in the regulation of body weight and insulin sensitivity.

    In obesity there is a progressive bias towards a pro-inflammatory T helper 1 (Th1) cell phenotype in fat which is associated with insulin resistance. In obesity, pro-inflammatory Th1 cell numbers substantially increase and there is a decline in the proportion of Foxp3+ Tregs, which are thought to exert anti-inflammatory effects in adipose tissue.  Recent reports indicate that Tregs have a role beyond classical modulation of the immune response; increasing evidence suggests that visceral adipose tissue CD4+ Foxp3+ Tregs may have a role to play in insulin sensitivity. Indeed, in obese AT, their proportion as well as their anti-inflammatory function is reduced drastically. The observed recruitment to, and expansion of, adipose tissue Th1 cells and decline in Tregs has been reported both obese mice and humans. Thus, in obesity, there are alterations in adipose tissue immune cell populations, which regulate the inflammatory environment and this impacts on energy balance and glucose homeostasis.

    Research in the Howard lab aim of the research is to understand the molecular basis of the role of the immune system and inflammation in obesity and insulin resistance using both in vitro and in vivo models. We have been particularly interested in the role of the immune cell transcription factor, T-bet in this process. Additional projects have looked at the role of T-bet in intestinal mucosal immune responses and mir142 as an immunometabolic regulator.


    Research interests (short)

    Immune and inflammatory pathways in the pathophysiology of obesity and insulin resistance.

    Expertise related to UN Sustainable Development Goals

    In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This person’s work contributes towards the following SDG(s):

    • SDG 2 - Zero Hunger
    • SDG 3 - Good Health and Well-being

    Education/Academic qualification

    Doctor of Philosophy, Leptin, starvation and the immune system, Imperial College London

    Award Date: 1 Jan 2002

    Master of Arts, University of Cambridge

    Award Date: 1 Jan 1992

    Bachelor of Medicine and Bachelor of Surgery, Distinctions Final MB Medicine (and specialities) and Final MB Pathology, University of Cambridge

    Award Date: 1 Jan 1990

    Bachelor of Arts, Natural Sciences/Medical Sciences Tripos, University of Cambridge

    Award Date: 1 Jan 1988

    Postdoctoral research, The role of suppressor of cytokine signalling 3 as a molecular mediator of leptin resistance, Harvard Medical School

    3 Jun 200325 Aug 2005


    • QP Physiology
    • RZ Other systems of medicine
    • obesity
    • metabolism
    • Inflammation
    • insulin resistance
    • Immunology
    • energy homeostasis
    • diabetes
    • immunometabolism
    • endocrinology


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