ViewpointDistribution of activated T cells migrating through the body: a matter of life and death
Section snippets
Short biography of naive, activated and memory T cells
T-cell precursors are released from the bone marrow into the blood (Fig. 1). These cells migrate to the thymus where they become thymocytes and undergo positive and negative selection. Each day about 1% are released as naive T cells into the periphery25.
Naive T cells continuously and randomly migrate through lymphoid and non-lymphoid organs (Fig. 1). Although naive T cells migrate back to both bone marrow and thymus26, 27, these organs are normally not considered their home, probably because
Preferential accumulation: increased proliferation and reduced cell death
The migration kinetics of activated T cells from two different sources (mLN and pLN) were recently investigated, including the analysis of cell proliferation and death19. T cells were activated via the T-cell receptor (TCR) and CD28, labelled, injected into rats and their localization within mLNs was analyzed19, 20. As expected21, 22, 23, 24, activated mLN T cells were found in significantly higher numbers in mLNs and the region drained by them (e.g. Peyer's patches and the lamina propria of
Perspectives
Activated T cells produce cytokines and express costimulatory molecules and can therefore induce the nonspecific proliferation of bystander lymphocytes40. Thus, the distribution of these potentially dangerous cells should be carefully regulated. Modifying the survival of activated T cells after random entry into the tissue represents an elegant way of making these cells available to the sites where they are needed, while retaining them in certain regions41. Such a mechanism might explain how
Conclusion
The current view on the regulation of lymphocyte migration postulates that preferences in lymphocyte distribution are mediated mainly during entry9, 12. Analyzing the migration of activated T cells, however, shifts the focus of this model by showing that preferential survival within the tissue is responsible for the preferential accumulation. It is unlikely that proliferation and death play a major role in the distribution of naive and memory T cells because the magnitude of migration7, 32 by
Unlinked list
51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61
Acknowledgements
We thank all our colleagues in the Dept of Functional and Applied Anatomy for their continuous support, especially K. Bankes, I. Dressendörfer, S. Lopez-Kostka, A. Reuße and F. Weidner. We gratefully acknowledge R. Pabst (Hannover), M. Schedlowski (Essen) and H. Westermann (Westermann & Partner, Hannover) for critical reading of the manuscript; M. Peter for help in preparing the figures; and S. Fryk for correcting the English. J.W. and U.B. were supported by the Deutsche Forschungsgemeinschaft
References (61)
- et al.
Immunol. Today
(1990) - et al.
Immunol. Today
(1996) Cell
(1991)- et al.
Lancet
(1994) Cell
(1994)- et al.
Blood
(1997) - et al.
Immunol. Today
(1995) - et al.
Adv. Immunol.
(1995) - et al.
Immunol. Today
(1996) - et al.
Cell. Immunol.
(1997)
Immunol. Today
Immunol. Today
Immunol. Today
Immunol. Today
J. Neuroimmunol.
Prog. Allergy
Immunol. Rev.
Lymphology
Trends Cell Biol.
Adv. Immunol.
Nature
Science
Science
J. Exp. Med.
J. Exp. Med.
Immunology
Eur. J. Immunol.
Eur. J. Immunol.
Eur. J. Immunol.
Eur. J. Immunol.
Cited by (71)
Nutritional Interventions to Reduce Immune Suppression Post Marathon
2014, Nutrition and Enhanced Sports Performance: Muscle Building, Endurance, and StrengthOxygen tension regulates NK cells differentiation from hematopoietic stem cells in vitro
2011, Immunology LettersCitation Excerpt :Immune cell development and activation occur in various lymphoid organs with different oxygen tensions [14,18]. Although developing NK cells can be exposed to both high and low oxygen conditions in the BM [16,18], it is not known whether exposure to different oxygen levels affect NK cell differentiation. Therefore, the hypothesis tested in this work was that oxygen conditions would affect on NK cell differentiation in vitro.
Patterns of leukocyte counts on admissions for acute heart failure - Presentation and outcome - Results from a community based registry
2011, International Journal of CardiologyCitation Excerpt :Previous studies hypothesized that the low relative lymphocyte count reflects activation of the hypothalamic–pituitary–adrenal axis. Serum cortisol and catecholamines were found elevated in patients with heart failure [30,36] and have been proposed responsible for shift in the leukocyte differential to a lower percentage of lymphocytes [32,33], lymphocyte apoptosis [37,38] down-regulation of proliferation and differentiation of lymphocytes [35] as well as homing of lymphocytes in lymphopoietical systems [39]. However, a recent study [24] in patients with heart failure failed to confirm a correlation between elevation of cortisol and relative reduction of lymphocyte count.
Intramuscular rather than oral administration of replication-defective adenoviral vaccine vector induces specific CD8<sup>+</sup> T cell responses in the gut
2007, VaccineCitation Excerpt :In fact, dendritic cells from the spleen or lymph node which do not induce gut-homing receptors can still prime T cells that migrate to the intestine and other non-lymphoid tissues in some experimental systems [34]. An alternative explanation for the induction of antigen-specific CD8+ T cells in the gut mucosa following i.m. immunization is that although anatomical sources of the antigen-presenting cells may be important for inducing site-specific CD8+ T cells [35], virus antigen may still be carried away and presented within the GALT and thus generate antigen-experienced CD8+ T cells that localize to the gut mucosa [33,36,37]. In fact, it is interesting that infection with a strictly respiratory virus such as the Sendai virus that infects locally can still generate antigen-specific CD8+ T cells in the gut mucosa or other non-lymphoid tissues [33].
The relative lymphocyte count on hospital admission is a risk factor for long-term mortality in patients with acute heart failure
2006, American Journal of Emergency Medicine