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In previous posts (The Thymus Gland - Part 1 and 2, Fri,15 Oct 2004) I have
proposed that the thymus gland, impaired by malabsorption due to celiac
disease, fails to sufficiently produce the regulatory T cells which help
the immune system decide whether to tolerate or attack foreign proteins or
antigens, thereby leading to or contributing to the numerous food
allergies, intolerances, and autoimmune conditions so frequently associated
with celiac disease.  The following study demonstrates just how important
the presence of properly selected regulatory T cells are in controlling
inflammatory processes by showing the appropriate regulatory T cells can
prevent colitis in mice.  Certain types of colitis (inflammation of the
large intestine) are associated with a high prevalence of celiac disease
(see second abstract below.)  An impaired thymus could be responsible for
this prevalence.

Recent studies have shown the prevalence of celiac disease in young
children is nearly identical to the prevalence of celiac disease in adults,
indicating that celiac disease has its origins during childhood.  Thymus
activity and production of T cells during childhood is especially critical
for the proper development of the immune system.  If the thymus is impaired
by malabsorption due to celiac disease during childhood, the stage may be
set for the development of future allergies, intolerences and autoimmune
responses.  The thymus, believed inactive after puberty, was only recently
(1999) shown to remain active throughout life into adulthood.  A diagnosis
of celiac disease which so typically occurs after age 40 may well indicate
the crucial repertoire of T cells produced by the thymus has already been
severely compromised.  It is imperative that the medical community screen
for and diagnose celiac disease during childhood at the earliest possible
stage.  A close look at how the thymus is affected by celiac disease is
highly warranted.

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Gut. 2005 Feb;54(2):207-14

Regulatory CD4+CD25+ cells reverse imbalances in the T cell pool of bone
marrow transplanted TG{varepsilon}26 mice leading to the prevention of
colitis.

Veltkamp C, Sartor RB, Giese T, Autschbach F, Kaden I, Veltkamp R, Rost D,
Kallinowski B, Stremmel W.

Department of Gastroenterology, University of Heidelberg, INF 410, 69120
Heidelberg, Germany. [log in to unmask]

BACKGROUND AND AIMS: Erroneous thymic selection of developing T lymphocytes
may be responsible for the expansion of self reactive T cells or may
contribute to the absence of regulatory T cells important in controlling
peripheral inflammatory processes. Colitis in bone marrow (BM) transplanted
Tgepsilon26 mice is induced by abnormally activated T cells developing in
an aberrant thymic microenvironment. We investigated the protective role of
regulatory CD4(+)CD25(+) T cells in this model. METHODS: BM from
(C57BL/6xCBA/J) F1 mice was transplanted into specific pathogen free
Tgepsilon26 mice (BM-->Tgepsilon26). Transplanted mice received no cells
(control), sorted CD4(+)CD25(+), or CD4(+)CD25(-) cells from mesenteric
lymph nodes (MLN) of normal mice. MLN cell subsets were analysed using
membrane markers. Cytokine secretion of MLN cells was measured using
intracellular cytokine staining and cytokine secretion in anti-CD3
stimulated cell cultures. Colitis was measured by histological scores.
RESULTS: CD4(+)CD25(+) cells were reduced in the MLNs of BM-->Tgepsilon26
mice. Transfer of regulatory CD4(+)CD25(+) but not of CD4(+)CD25(-) cells
reduced the number of MLN CD4(+) T cells in BM-->Tgepsilon26 recipients and
increased the number of MLN CD8(+) cells, thereby normalising the CD4(+)/CD8
(+) ratio. CD4(+)CD25(+) but not CD4(+)CD25(-) cell transfer into BM--
>Tgepsilon26 mice reduced the number of tumour necrosis factor alpha(+) CD4
(+) cells and increased the secretion of transforming growth factor beta by
MLN cells. Transfer of 3x10(5) CD4(+)CD25(+) cells after BM transplantation
into Tgepsilon26 mice prevented colitis whereas CD4(+)CD25(-) cells had no
protective effect. CONCLUSIONS: These results suggest that defective
selection or induction of regulatory T cells in the abnormal thymus is
responsible for the development of colitis in BM-->Tgepsilon26 mice.
Transfer of CD4(+)CD25(+) cells can control intestinal inflammation in BM--
>Tgepsilon26 mice by normalising the number and function of the MLN T cell
pool.

PMID: 15647183 [PubMed - in process]

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Scand J Gastroenterol. 2004 Sep;39(9):837-45

Clinical characteristics of collagenous and lymphocytic colitis.

Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK.

Department of Internal Medicine, University of Oulu, OYS, PO Box 20, FIN-
90029 Oulu, Finland. [log in to unmask]

BACKGROUND: Microscopic colitides (MC), collagenous colitis (CC) and
lymphocytic colitis (LC) share clinical features, but their mutual
relationship is unclear, and clinical comparative studies are rare. We
aimed to examine the clinical features in CC and LC by focusing on
concomitant diseases. METHODS: Patients with MC (30 with CC, 54 with LC)
were identified in the pathology databases and by reviewing biopsies.
Controls included 84 age- and sex-matched persons. The clinical data
collected from patient records were prospectively completed by interviews.
RESULTS: The female:male ratio was 2:1 in CC and 5.75:1 in LC. Mean age at
diagnosis was 53 in CC and 55.4 years in LC. There were no differences in
the pattern of symptoms. Concomitant autoimmune diseases were more common
in CC (53.3%) than in LC (25.9%; P = 0.017). Celiac disease was common in
both CC (20%) and LC (14.8%). Bronchial asthma was associated with LC
(25.9%), but not with CC (6.7%; P = 0.042). Colon diverticulosis was rare
in MC (16%) compared with the controls (39%; P = 0.001). Hypolactasia was
common in MC (45%; 76% in CC, 54% in LC) compared to its prevalence in the
Finnish general population (17%). CONCLUSIONS: CC and LC are largely
similar clinically, but the differences in the occurrence of autoimmune
conditions and bronchial asthma suggest that they differ in
immunopathogenesis. MC is associated with reduced lactose tolerance and
shows a negative association with diverticular disease, possibly related to
the small intestinal pathology and abnormal stool consistency.

PMID: 15513381 [PubMed - indexed for MEDLINE]

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