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Meeting Report

Review of the 1st Annual World Congress of Immunodiseases and Therapeutics

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Pages 757-759 | Published online: 10 Jan 2014

Abstract

BIT’s 1st Annual World Congress of Immunodiseases and Therapeutics was held in Beijing, China, on 15–17 May 2010. The meeting provided a venue for a wide spectrum of researchers in the basic sciences and clinical areas to present and share their data and ideas. The pervading theme of the meeting dealt with the concept that immune mechanisms underlie most, if not all, medical diseases and therefore the future of medical therapeutics necessitates a greater understanding and corrective manipulation of dysfunctional metabolic and immune pathways. The meeting was well run, educational and enjoyable.

BIT’s 1st Annual World Congress of Immuno diseases and Therapeutics was held in Beijing, China, on 15–17 May 2010. As judged by comments from the participants, it was a highly successful meeting that covered a broad spectrum of immune-related subjects. The organizers adopted an unconventional approach to organizing the meeting that certainly did not guarantee success beforehand but, in retrospect, may be the preferable way to facilitate the spread of new ideas and information. BIT Life Sciences is a private organization that charged the speakers the full registration fee. Scientists who had published in journals were invited to speak and were given a forum to share their ideas with others, but the registration fee may have dissuaded many from attending. However, the end result was that the majority of the approximately 300 attendees were speakers genuinely interested in their message. The group appeared to mainly consist not of the older established researchers but rather of mid-career individuals immersed in the productive activities of their careers. The real value of most meetings lies in the establishment of collaborative relationships and this venue did a superb job of catalyzing these relationships by selecting people to attend who were actively involved in advancing their research.

The program lasted for 3 days. The first half day was devoted to four keynote lectures given by established researchers from Canada, Switzerland and the USA, followed by 138 20-min talks given over the next 2 and a half days. A poster session completed the academic portion of the meeting. The strength of the meeting resided in the broad spectrum and quality of the lectures. Topics ranged from research on individual molecules to the systems biology approach, emphasizing the functional modules found in biologic complex adaptive systems. Clinical lectures on related medical diseases brought focus to the meeting.

The lectures were organized into six sessions that were delivered in two to four concurrent sessions. It is impossible to give due justice to all the speakers in a short article. Therefore, out of necessity, we will confine the following comments to just a few of the many high points of the meeting.

As mentioned, much of the value of these meetings resides in the cross-pollination of ideas, the realization that others are arriving at the same conclusions despite coming at a given problem from different approaches, and the collaborative relationships that are formed. Four consecutive seemingly unrelated lectures provide an excellent example. Sergey Suchkov (Sechenov Moscow Medical Academy, Moscow, Russia) suggested a unifying paradigm for considering idiopathic inflammatory/autoimmune disorders manifesting in different organs Citation[1]. He reported on his work evaluating the immunological parameters associated with the chronic inflammatory conditions of postinfectious pyelonephritis, intracranial infectious and inflammatory pathologies, myocarditis and chronic obstructive pulmonary disease, all of which had underlying immune pathologies. He divided the immune pathologies into the following categories: postinfectious immune deficiency; postinfectious autoimmunity; and postinfectious immune deficiency with autoimmunity. Inherent in his work was the association of immune deficiencies with chronic inflammation. Rateb from Cairo, Egypt, followed and discussed her work involving the influence of estrogen and progesterone steroid signaling on innate and adaptive immunity. Her talk emphasized the importance of different known steroids on the immune system and how little we know about the effects of the lesser known steroid/steroid receptor family on immunity. William Chamberlin (Texas Tech Medical Center, TX, USA) followed and presented the concepts championed by Anthony Segal (University College London, London, UK) Citation[2] and Marcel Behr (McGill University Health Centre, QC, Canada) Citation[3] suggesting that Crohn’s disease is not an autoimmune disease in the usual sense but is in fact associated with innate immune deficiency – both genetic and acquired. The association of innate immune deficiency with an underlying chronic intracellular infection was briefly mentioned but not stressed. He emphasized that Crohn’s disease should therefore be treated best with an agent that enhances innate immunity, downregulates inappropriate, ineffectual inflammation and strengthens overall immunity rather than using the conventional approaches of suppressing immunity. He presented evidence taken from clinical trials in HIV/AIDS, malaria and TB demonstrating that 16-α bromoepiandrosterone displayed these qualities and may offer a new approach to treating inflammatory bowel disease Citation[4–6]. Joss Langhorst (University of Duisburg-Essen, Essen, Germany) then presented his work showing impairment of innate immunity as manifested by the diminished production of α and β defensins from the ileum and colon in Crohn’s disease. He speculated that decreased defensin levels lead to a weakened intestinal barrier function against intestinal microbes and might be crucial to the pathophysiology of Crohn’s disease. Similar to the conclusions reached by the previous speakers, he concluded that enhancing innate immunity would be beneficial for Crohn’s disease patients.

Langhorst also noted that irritable bowel syndrome patients have elevated defensin levels, suggesting that irritable bowel syndrome is associated with an activation of the innate immune system, and implying that it is in fact an inflammatory disease without macroscopic evidence of inflammation Citation[7].

Such a serendipitous sequencing of seemingly unrelated talks has already spawned an international collaborative effort that may impact on the treatment of inflammatory bowel disease. Whether successful or not, the way in which the organizers arranged this meeting encouraged such collaborative efforts.

The talk by Nicola Cirillo (University of Bristol, Bristol, UK) perhaps best exemplifies how theoretic and cutting-edge some of the lectures were Citation[8]. His lecture was entitled ‘Merging high-throughput techniques and multiparametric image analysis to find the mechanisms causally involved in skin autoimmune disease’. His approach utilizes the principles of complexity science and employs them to gain a better understanding of the complex adaptive systems found in the molecular networks of biology. He was asked to describe his approach in his own words:

In accord with a system biological approach, we used the autoimmune skin blistering disease pemphigus vulgaris as a model of external perturbation of the cell, where the perturbation is represented by patients’ autoantibodies/sera and the biological system studied is the adhesion machinery of keratinocytes. The central idea of this research is to combine the information gained by high-throughput techniques, namely DNA and antibody microarrays and siRNA screening, with an in silico theoretical analysis.

There are four main steps in this approach:

  • • Analytical-predictive phase: systems biology modeling and network analysis are employed that will serve to predict putative key molecules and provide a framework for studying the changes in the system after perturbation;

  • • Experimental phase: high-throughput screening of the molecular response of the system subject to perturbation (e.g., autoantibodies);

  • • Synthesis phase: in silico and experimental data are integrated. This process leads to the selection of a limited number of molecules to be extensively examined for their predicted ability to reduce/prevent the changes triggered by the perturbation. These molecules can then be targeted, for example, for therapeutic purposes;

  • • Implementation phase: the results gained in the synthesis phase are in turn used to enrich the initial system (phase 1) in terms of what its molecular constituents are, with which molecules they interact and how these interactions lead to cell function; the results may also lead to a spatio–temporal molecular characterization of the system. Finally, this phase provides information about the reliability of predictive biological/biophysical parameters.

In his talk, Cirillo showed how this approach led to the discovery of the crucial role of plakophilin 3, a cell adhesion molecule occurring in desmosomes, in the pathogenesis of pemphigus vulgaris (PV). In line with a systems level approach, he also combined siRNA screening and multiparametric image analysis to find the biomodules (loose associations of preferred molecular interaction partners that interact to perform a collective function) responsible for specific apoptotic cell features induced by PV sera. This laid the foundations for new specific therapies for PV and highlighted the huge translational potential of systems biology.

In summary, this meeting provided a platform for many stimulating, provocative talks covering a wide range of immune-related subjects. We should all look forward to BIT’s 2nd Annual World Congress of Immunodiseases and Therapeutics.

Financial & competing interests disclosure

William Chamberlin owns shares in Harbor Biosciences, CA, USA. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

References

  • Suchkov S. Postinfectious clinical and immune-mediated syndrome as a major factor in the chronization and progression of the infectious diseases. Presented at: BIT Life Sciences 1st Annual World Congress of Immunodiseases and Therapeutics. Beijing, China, 15–17 June 2010.
  • Hayee B, Rahman F, Sewell G, Smith A, Segal A. Crohn’s disease as an immunodeficiency. Expert Rev. Clin. Immunol.6(4), 585–596 (2010).
  • Lalande J, Behr M. Mycobacteria in Crohn’s disease: how innate immune deficiency may result in chronic inflammation. Expert Rev. Clin. Immunol.6(4), 633–641 (2010).
  • Reading C, Dowding C, Schramm B et al. Improvement in immune parameters and human immunodeficiency virus-1 viral response in individuals teated with 16α-bromoepiandrosterone (HE2000). Clin. Microbiol. Infect.12, 1082–1088 (2006).
  • Stickney D, Noveljic Z, Garsd A, Destiche D, Frincke J. Safety and activity of the immune modulator HE2000 on the incidence of tuberculosis and other opportunistic infection in AIDS patients. Antimicrob. Agents Chemother.51(7), 2639–2641 (2007).
  • Conrad N, Wang A, Pieters R et al. 16α-Bromoepiandrosterone (HE2000) limits non-productive inflammation and stimulates immunity in lungs. Clin. Exp. Immunol.158(3), 308–316 (2009).
  • Langhorst J, Wieder A, Michalsen A, Musial F, Dobos GJ, Rueffer A. Activated innate immune system in irritable bowel system. Gut56, 1325–1326 (2007).
  • Cirillo N, Prime SS. Desosomal interactome in keratinocytes: a systems biology approach leading to an understanding of the pathogenesis of skin disease. Cell. Mol. Life Sci.66(21), 3517–3533 (2009).

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