<p class="first" id="P2">The Resistin-Like Molecules (RELM) α, β, and γ and their
namesake, resistin, share
structural and sequence homology but exhibit significant diversity in expression and
function within their mammalian host. RELM proteins are expressed in a wide range
of diseases, such as: microbial infections (eg. bacterial and helminth), inflammatory
diseases (eg. asthma, fibrosis) and metabolic disorders (eg. diabetes). While the
expression pattern and molecular regulation of RELM proteins are well characterized,
much controversy remains over their proposed functions, with evidence of host-protective
and pathogenic roles. Moreover, the receptors for RELM proteins are unclear, although
three receptors for resistin, decorin, adenylyl cyclase-associated protein 1 (CAP1),
and Toll-like Receptor 4 (TLR4) have recently been proposed. In this review, we will
first summarize the molecular regulation of the RELM gene family, including transcription
regulation and tissue expression in humans and mouse disease models. Second, we will
outline the function and receptor-mediated signaling associated with RELM proteins.
Finally, we will discuss recent studies suggesting that, despite early misconceptions
that these proteins are pathogenic, RELM proteins have a more nuanced and potentially
beneficial role for the host in certain disease settings.
</p>