Role of CD53 in leukocyte trafficking
presented by Ms Louisa Yeung, Postgraduate Student, CID
Under an inflammatory
setting, immune cells require the ability to migrate from the blood to sites of
infection in order to mount an immune response. Aberrant leukocyte migration is
a major contributor to the development of inflammatory and autoimmune disease
such as rheumatoid arthritis. Here, cellular infiltrates, result in a
microenvironment rich in inflammatory cytokines. Leukocyte recruitment requires the actions
of adhesion molecules and their associated ligands. Tetraspanins are a
superfamily of transmembrane proteins that promote the formation of association
networks known as tetraspanin-enriched microdomains (TEMs), in which molecules
such as leukocyte integrins form associations with a range of other
proteins. The leukocyte-expressed tetraspanin CD53 has recently been
identified as a potential regulator of leukocyte recruitment. Though the
mechanism by which CD53 accomplishes this remains unknown, unpublished data
suggest that it may occur through the regulation of L-selectin expression. In
the scope of inflammation and disease, L-selectin contributes to leukocyte
tethering and rolling during the initial steps of recruitment, and is a
fundamental molecule involved during lymphocyte homing. Thus, failure of
adhesion molecule function and/or associated downstream signalling at this
phase in the recruitment cascade may restrict the leukocyte recruitment
response.
and
Regulatory T cell interactions with the vascular
endothelium
presented by Prof Michael Hickey,
NHMRC Senior Research Fellow, CID
Michael Hickey is an
NHMRC Senior Research Fellow, and head of the leukocyte trafficking group in
the CID. Regulatory
T cell (Treg) trafficking to inflamed sites in the periphery is a critical
element in the capacity of regulatory T cells to control inflammation. For
Tregs to enter sites of inflammation from the circulation, they must undergo a
sequence of interactions in the microvasculature of the target tissue. This presentation
will describe research performed over the last few years using Treg reporter
mice and intravital microscopy, examining the interactions between Tregs and
the inflamed microvascular endothelium in the skin, in a model of T
cell-dependent skin inflammation.
A
light lunch is served prior to the seminar at 11:45am in the seminar room
foyer, level 2, TRF Building.
Further
information available from CID Weekly Seminar Series website [http://www.med.monash.edu.au/scs/medicine/cid/seminar-series.html]
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