Transcript Slide 1 - AccessPhysiotherapy

Proposed pathogenesis of inflammatory bowel disease and target sites for pharmacological intervention. Shown are the interactions among bacterial
antigens in the intestinal lumen and immune cells in the intestinal wall. If the epithelial barrier is impaired, bacterial antigens can gain access to antigenpresenting cells (APC) such as dendritic cells in the lamina propria. These cells then present the antigen(s) to CD4+ lymphocytes and also secrete
cytokines such interleukin (IL)-12 and IL-18, thereby inducing the differentiation of TH1 cells in Crohn disease (or, under the control of IL-4, type 2 helper T
cells [TH2] in ulcerative colitis). The balance of pro-inflammatory and anti-inflammatory events is also governed by regulatory TH17 and TReg cells, both of
which serve to limit immune and inflammatory responses in the GI tract. Transforming growth factor (TGF)β and IL-6 are important cytokines that drive the
Source: INFLAMMATORY BOWEL DISEASE, The Color Atlas of Physical Therapy
expansion of the regulatory T cell subsets. The TH1 cells produce a characteristic array of cytokines, including interferon (IFN)γ and TNFα, which in turn
Citation: Shamus
E. The Color
Atlasregulate
of Physical
2015 Available
at: http://mhmedical.com/
Accessed:
April Recruitment
08, 2017
activate macrophages.
Macrophages
positively
TH1 Therapy;
cells by secreting
additional
cytokines, including IFNγ
and TNFα.
of a variety of
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leukocytes is mediated by activation of resident immune cells including neutrophils. Cell adhesion molecules such as integrins are important in the
infiltration of leukocytes and novel biological therapeutic strategies aimed at blocking leukocyte recruitment are effective at reducing inflammation. General
immunosuppressants (e.g., glucocorticoids, thioguanine derivatives, methotrexate, and cyclosporine) affect multiple sites of inflammation. More site-