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Immunology 2018

J u l y 0 5 - 0 7 , 2 0 1 8

V i e n n a , A u s t r i a

Page 104

Journal of Clinical Immunology and Allergy

ISSN 2471-304X

1 5

t h

I n t e r n a t i o n a l C o n f e r e n c e o n

Immunology

I

nflammatory processes such as those promoting atherosclerotic lesion formations are pivotally driven by components of the

innate and adaptive immune axis. Chemokines and their receptors are particularly prominent part of the innate immune arm.

While the role of classical chemokines, i.e., belonging to the CC or CXC families is increasingly well understood, an emerging family

of chemokine like inflammatory mediators termed innate chemokines, CLF chemokines or micro-chemokines, which additionally

structurally and functionally overlaps with the mediator class of alarmins, has been identified, but it yet has to be comprehensively

characterized regarding its molecular mechanism and role in disease. For example, innate chemokines modulate inflammatory

reactions in the atherogenic arterial wall and numerous other inflamed tissues, but the precise receptor signaling mechanisms are

still only poorly understood. What is known is that many innate chemokines share functional homology with classical chemokines

and signal through classical chemokine receptors, whereas they do not exhibit conserved structural features such as N-terminal

tandem cysteine residues or the chemokine fold. Thus, important receptor bindingmotifs yet have to be characterized. This lecture

will give an overview of the mechanisms underlying molecular hijacking of classical chemokine receptors by innate chemokines,

featuring their pathophysiological role. Examples will encompass high mobility group binding protein-1 (HMGB1), macrophage

migration inhibitory factor (MIF), MIF-2/D-D (D dopachrome tautumerase) T and certain β-defensins. Receptor usage, binding

domains, signalling, innate immune cell regulation and involvement in various inflammatory conditions, including atherosclerosis

will be discussed. The lecture will outline strategies to target such mediators in disease either in conjunction or explicit exclusion

of the co-targeting of classical chemokines. Finally, a cross kingdom analysis will be shared offering more general understanding

of some of these mediators.

juergen.bernhagen@med.uni-muenchen.de

MIF proteins as prototypical innate chemokines in

inflammatory and cardiovascular disease

Jurgen Bernhagen

1, 2

1

Ludwig-Maximilians University of Munich, Germany

2

University of London, UK

Insights Allergy Asthma Bronchitis 2018, Volume: 4

DOI: 10.21767/2471-304X-C1-003