T cells at the turn of the twenty-first century
β Scribed by Lucy R Wedderburn; Lee Dianda
- Publisher
- Elsevier Science
- Year
- 2000
- Tongue
- English
- Weight
- 155 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0167-5699
No coin nor oath required. For personal study only.
β¦ Synopsis
he Cellular Immunology Unit (CIU) in Oxford, UK, has recently celebrated 36 years of pioneering work in cellular immunology. As part of this celebration, a recent meeting brought together others in the field, to discuss the current understanding of T-cell biology as we begin a new millennium.
Homing directions
Leukocyte recirculation is facilitated by the cells rolling over high endothelial venules (HEVs) 1 . Although the shear stress of the cell wall varies greatly between anatomical sites, as well as in response to exercise or inflammation, the rate of leukocyte rolling remains almost constant (T. Springer, Boston, MA). This is facilitated by an increase in the number of bonds between selectins and their ligands (located on microvilli tips). In addition, the number of microvilli tethers is increased where high shear stress occurs. This 'braking system' permits attachment under conditions of high shear stress; by contrast, under conditions of low stress or high ligand density, leukocytes do not become stalled.
J. Hopkin (Oxford) described a family practitioner study of 2000 children in Oxfordshire, UK, which examined the links between childhood infections, maternal atopy, social factors and childhood allergy. Pertussis vaccination and infections in the first two years of life emerged as strong predictors of atopy. The odds ratio for infections increased dramatically if antibiotics were given; antibiotic use in early life may provide the link between increased allergy and 'infection' in this study. Commensal organisms seem crucial for maturation of antigen-specific T cells, perhaps explaining the adverse effect of some antibiotics (simple penicillins seem not to be associated with atopy). In animal models, gut decontamination can induce Th2-biased responses.
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