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with a Th2-Associated Expression Pattern1
Klinik und Poliklinik für Dermatologie, Universitätsklinikum Benjamin Franklin, Freie Universitat Berlin, Berlin, Germany
We have cloned a novel human CC-chemokine, alternative macrophage
activation-associated CC-chemokine (AMAC)-1. The isolated cDNA clone
(803 bp) shows a single open reading frame of 267-bp coding for 89
amino acid residues; mature AMAC-1 protein is predicted to consist of
69 amino acids with a m.w. of 7855. Sequence alignment and 3D-modeling
show the typical structural characteristics of CC-chemokines with
special features in the receptor-activating domain. AMAC-1 is most
closely related to MIP-1
with a cDNA and protein sequence homology
of 55% and 59%, respectively. However, the expression pattern of
AMAC-1 is directly opposite to that of MIP-1. While MIP-1 is
induced by classical macrophage mediators such as LPS and is inhibited
by IL-4 and glucocorticoids, AMAC-1 is specifically induced in
macrophages by alternative macrophage mediators such as IL-4, IL-13,
and IL-10. Expression of AMAC-1 is inhibited by IFN-
while
glucocorticoids exert a slightly positive synergistic effect in
combination with IL-4. Peripheral blood monocytes do not express
AMAC-1; time course experiments show that monocyte-to-macrophage
differentiation is a prerequisite for AMAC-1 expression. Expression of
AMAC-1 by granulocyte--macrophage CSF/IL-4-induced, monocyte-derived
dendritic cells is complex; in mature adherent dendritic cells,
however, only minor AMAC-1 mRNA expression was found. In vivo, AMAC-1
is expressed by alveolar macrophages from healthy persons, smokers, and
asthmatic patients. In conclusion, AMAC-1 is a novel CC-chemokine whose
expression is induced in alternatively activated macrophages by
Th2-associated cytokines; thus, AMAC-1 may be involved in the
APC-dependent T cell development in inflammatory and immune
reactions.
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