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The triggering receptor expressed on myeloid cells (TREM) in inflammatory bowel disease pathogenesis.

Genua M, Rutella S, Correale C, Danese S - J Transl Med (2014)

Bottom Line: In the intestine, TREM-1 is highly expressed by macrophages, contributing to inflammatory bowel disease (IBD) pathogenesis.Contrary to current understanding, TREM-2 also promotes inflammation in IBD by fueling dendritic cell functions.This review will focus specifically on recent insights into the role of TREM proteins in IBD development, and discuss opportunities for novel treatment approaches.

View Article: PubMed Central - PubMed

Affiliation: IBD Center, Humanitas Clinical and Research Hospital, Rozzano, Italy. marco.genua@humanitasresearch.it.

ABSTRACT
The Triggering Receptors Expressed on Myeloid cells (TREM) are a family of cell-surface molecules that control inflammation, bone homeostasis, neurological development and blood coagulation. TREM-1 and TREM-2, the best-characterized receptors so far, play divergent roles in several infectious diseases. In the intestine, TREM-1 is highly expressed by macrophages, contributing to inflammatory bowel disease (IBD) pathogenesis. Contrary to current understanding, TREM-2 also promotes inflammation in IBD by fueling dendritic cell functions. This review will focus specifically on recent insights into the role of TREM proteins in IBD development, and discuss opportunities for novel treatment approaches.

No MeSH data available.


Related in: MedlinePlus

The TREM gene cluster in mice and humans. Schematic diagram that compares the order of genes in the TREM clusters in humans (A) and mice (B). Genes encoding TREM protein were drawn in orange, whereas TREM-like genes are depicted in red. Models of the encoded proteins are shown below the corresponding genes. The DAP12 adaptor is also shown with its ITAM. TLT proteins are shown with the corresponding ITIM.
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Fig1: The TREM gene cluster in mice and humans. Schematic diagram that compares the order of genes in the TREM clusters in humans (A) and mice (B). Genes encoding TREM protein were drawn in orange, whereas TREM-like genes are depicted in red. Models of the encoded proteins are shown below the corresponding genes. The DAP12 adaptor is also shown with its ITAM. TLT proteins are shown with the corresponding ITIM.

Mentions: Currently, the human TREM gene cluster (Figure 1A) includes several other members, namely the TREM-like transcripts −1, −2, -3, and −4 (TREML1, TREML2, TREML3 and TREML4). The murine gene cluster (Figure 1B) however did not include NKp44, but did contain genes encoding for the plasmacytoid-dendritic cell Trem (pDC-Trem), Treml −1, −2, −4 and −6, and Trem3. This latter gene was found also in the human cluster as a non-transcriptionally active pseudo-gene [3]. It is important to note that while both the murine and human gene clusters cover many putative coding sequences (reviewed in [4], Figure 1), protein products have been discovered and characterized only for few genes, as discussed below.Figure 1


The triggering receptor expressed on myeloid cells (TREM) in inflammatory bowel disease pathogenesis.

Genua M, Rutella S, Correale C, Danese S - J Transl Med (2014)

The TREM gene cluster in mice and humans. Schematic diagram that compares the order of genes in the TREM clusters in humans (A) and mice (B). Genes encoding TREM protein were drawn in orange, whereas TREM-like genes are depicted in red. Models of the encoded proteins are shown below the corresponding genes. The DAP12 adaptor is also shown with its ITAM. TLT proteins are shown with the corresponding ITIM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4231187&req=5

Fig1: The TREM gene cluster in mice and humans. Schematic diagram that compares the order of genes in the TREM clusters in humans (A) and mice (B). Genes encoding TREM protein were drawn in orange, whereas TREM-like genes are depicted in red. Models of the encoded proteins are shown below the corresponding genes. The DAP12 adaptor is also shown with its ITAM. TLT proteins are shown with the corresponding ITIM.
Mentions: Currently, the human TREM gene cluster (Figure 1A) includes several other members, namely the TREM-like transcripts −1, −2, -3, and −4 (TREML1, TREML2, TREML3 and TREML4). The murine gene cluster (Figure 1B) however did not include NKp44, but did contain genes encoding for the plasmacytoid-dendritic cell Trem (pDC-Trem), Treml −1, −2, −4 and −6, and Trem3. This latter gene was found also in the human cluster as a non-transcriptionally active pseudo-gene [3]. It is important to note that while both the murine and human gene clusters cover many putative coding sequences (reviewed in [4], Figure 1), protein products have been discovered and characterized only for few genes, as discussed below.Figure 1

Bottom Line: In the intestine, TREM-1 is highly expressed by macrophages, contributing to inflammatory bowel disease (IBD) pathogenesis.Contrary to current understanding, TREM-2 also promotes inflammation in IBD by fueling dendritic cell functions.This review will focus specifically on recent insights into the role of TREM proteins in IBD development, and discuss opportunities for novel treatment approaches.

View Article: PubMed Central - PubMed

Affiliation: IBD Center, Humanitas Clinical and Research Hospital, Rozzano, Italy. marco.genua@humanitasresearch.it.

ABSTRACT
The Triggering Receptors Expressed on Myeloid cells (TREM) are a family of cell-surface molecules that control inflammation, bone homeostasis, neurological development and blood coagulation. TREM-1 and TREM-2, the best-characterized receptors so far, play divergent roles in several infectious diseases. In the intestine, TREM-1 is highly expressed by macrophages, contributing to inflammatory bowel disease (IBD) pathogenesis. Contrary to current understanding, TREM-2 also promotes inflammation in IBD by fueling dendritic cell functions. This review will focus specifically on recent insights into the role of TREM proteins in IBD development, and discuss opportunities for novel treatment approaches.

No MeSH data available.


Related in: MedlinePlus