The Genetics of Inflammatory Bowel Disease

[Guest guest]

Dear All;

A good review was published today, describing some of the exciting

progress being made in inflammatory bowel disease genetics. I was

particularly pleased to see coverage of the roles of IL-23, Th17

cells and IL-17 in the inflammation process (see Figure 3 of the full

paper, which I will post soon).

_______________

Am J Gastroenterol. 2007 Sep 25 [Epub ahead of print]

The Genetics of Inflammatory Bowel Disease.

Van Limbergen J, RK, Nimmo ER, Satsangi J

Gastrointestinal Unit, Molecular Medicine Centre, Western General

Hospital, University of Edinburgh, Edinburgh, United Kingdom.

Great progress in the understanding of the molecular genetics of

inflammatory bowel disease (IBD) has been made over the last 10

years. Strong epidemiological evidence, based initially on

concordance data in twin/family studies, led to the application of

genome-wide linkage analysis involving multiply affected families and

the identification of a number of susceptibility loci. Further

characterization of the IBD1 locus on chromosome 16 led to the

discovery of the NOD2/CARD15 gene as the first susceptibility gene in

Crohn's disease for 2001. This landmark finding has led to a

redirection of basic research in IBD with interest focused

principally on regulation of the innate immune response and mucosal

barrier function. Within the last year, the use of genome-wide

association studies has provided new insights into primary

pathogenetic mechanisms; several new genes such as the Interleukin-23

receptor (IL23R) and ATG16L1 (autophagy-related 16-like 1) genes are

strongly implicated. Overall, these studies promise to change our

fundamental understanding of IBD pathophysiology and to have

implications for clinical practice. PMID: 17894847.

_______________

Not included in this review is the more recent evidence for the role

of retinoic acid in regulating the switch between inflammatory Th17

cells and anti-inflammatory regulatory T cells (Tregs), and

imprinting the Tregs with gut-homing characteristics, but hopefully

it will get IBD (and PSC) researchers thinking outside of the Th1/Th2

box?

Best regards,

Dave

(father of (23); PSC 07/03; UC 08/03)

[Guest guest]

Thanks for the good news Dave. We all love to see progress like

this research.

Ricky

PSC 2003

From:

[mailto: ] On Behalf

Of

Sent: Thursday, September 27, 2007 9:52 PM

To:

Subject: The Genetics of Inflammatory Bowel Disease

Dear All;

A good review was published today, describing some of the exciting

progress being made in inflammatory bowel disease genetics. I was

particularly pleased to see coverage of the roles of IL-23, Th17

cells and IL-17 in the inflammation process (see Figure 3 of the full

paper, which I will post soon).

_______________

[Guest guest]

Hi Dave,Thanks for keeping us up on the latest. If Partners should start some seed grants, is it possible to make a specific seed grant, say to look into the role of retinoic acid in regulating the switch between Th17 cells and T cells?Can we plant the seed to get them thinking outside the box?Lee Not included in this review is the more recent evidence for the role of retinoic acid in regulating the switch between inflammatory Th17 cells and anti-inflammatory regulatory T cells (Tregs), and imprinting the Tregs with gut-homing characteristics, but hopefully it will get IBD (and PSC) researchers thinking outside of the Th1/Th2 box?Best regards,Dave (father of (23); PSC 07/03; UC 08/03)

[Guest guest]

Thanks a lot, , highly interesting!

-- In , " " wrote:

>

> Dear All;

>

> A good review was published today, describing some of the exciting

> progress being made in inflammatory bowel disease genetics. I was

> particularly pleased to see coverage of the roles of IL-23, Th17

> cells and IL-17 in the inflammation process (see Figure 3 of the full

> paper, which I will post soon).

> _______________

..> Not included in this review is the more recent evidence for the role

> of retinoic acid in regulating the switch between inflammatory Th17

> cells and anti-inflammatory regulatory T cells (Tregs), and

> imprinting the Tregs with gut-homing characteristics, but hopefully

> it will get IBD (and PSC) researchers thinking outside of the Th1/Th2

> box?

>

I agree, and hopefully many enough will be looking " round the corner " to get a

more

complete view!

Best regards,

[Guest guest]

Thanks, I honestly don't understand it, but it sounds promising.

>

> Dear All;

>

> A good review was published today, describing some of the exciting

> progress being made in inflammatory bowel disease genetics. I was

> particularly pleased to see coverage of the roles of IL-23, Th17

> cells and IL-17 in the inflammation process (see Figure 3 of the

full

> paper, which I will post soon).

> _______________

>

> Am J Gastroenterol. 2007 Sep 25 [Epub ahead of print]

>

> The Genetics of Inflammatory Bowel Disease.

>

> Van Limbergen J, RK, Nimmo ER, Satsangi J

>

> Gastrointestinal Unit, Molecular Medicine Centre, Western General

> Hospital, University of Edinburgh, Edinburgh, United Kingdom.

>

> Great progress in the understanding of the molecular genetics of

> inflammatory bowel disease (IBD) has been made over the last 10

> years. Strong epidemiological evidence, based initially on

> concordance data in twin/family studies, led to the application of

> genome-wide linkage analysis involving multiply affected families

and

> the identification of a number of susceptibility loci. Further

> characterization of the IBD1 locus on chromosome 16 led to the

> discovery of the NOD2/CARD15 gene as the first susceptibility gene

in

> Crohn's disease for 2001. This landmark finding has led to a

> redirection of basic research in IBD with interest focused

> principally on regulation of the innate immune response and mucosal

> barrier function. Within the last year, the use of genome-wide

> association studies has provided new insights into primary

> pathogenetic mechanisms; several new genes such as the Interleukin-

23

> receptor (IL23R) and ATG16L1 (autophagy-related 16-like 1) genes

are

> strongly implicated. Overall, these studies promise to change our

> fundamental understanding of IBD pathophysiology and to have

> implications for clinical practice. PMID: 17894847.

> _______________

>

> Not included in this review is the more recent evidence for the

role

> of retinoic acid in regulating the switch between inflammatory Th17

> cells and anti-inflammatory regulatory T cells (Tregs), and

> imprinting the Tregs with gut-homing characteristics, but hopefully

> it will get IBD (and PSC) researchers thinking outside of the

Th1/Th2

> box?

>

> Best regards,

>

> Dave

> (father of (23); PSC 07/03; UC 08/03)

>